Immuno E1 MCQ

Most T lymphocytes have a dual specificity for which one of the following pairs of molecules? A. A particular allelic form of a major histocompatibility complex (MHC) molecule and a peptide bound to the MHC molecule B. Both MHC class I and class II molecules C. Both peptide and glycolipid antigens D. Both soluble peptides and peptide-MHC complexes E. MHC molecules and CD4 or CD8

A. A particular allelic form of a major histocompatibility complex (MHC) molecule and a peptide bound to the MHC molecule

A helper T cell response to a protein antigen requires the participation of antigen-presenting cells that express which of the following types of molecules? A. Class II MHC and costimulators B. Class I MHC and CD4 C. Class II MHC and CD8 D. CD4 and costimulators E. Class II MHC and CD4

A. Class II MHC and costimulators

A 2-year-old boy suffers from recurrent bacterial infection of his ears, sinuses, lungs, and skin; laboratory studies indicate absence of sialylated Lewis X on his leukocytes. He is diagnosed with leukocyte adhesion deficiency type 2 (LAD-2). Which type of adhesive interaction required for leukocyte migration is defective in this boy? A. E-selectin ligand binding to E-selectin B. CD4 binding to class II MHC C. VLA-4 binding to VCAM-1 D. Ig Fc receptor binding to Ig-coated cells E. LFA-1 binding to ICAM-1

A. E-selectin ligand binding to E-selectin

Which one of the following statements about dendritic cells is true? A. Immature dendritic cells are ubiquitously present in skin and mucosal tissues. B. Dendritic cell maturation occurs after migration to lymph nodes in response to signals derived from activated T cells. C. Class II MHC and T cell costimulators are highly expressed on immature dendritic cells and are down-regulated during maturation. D. Dendritic cells that enter lymph nodes through draining lymphatics migrate to the B cell-rich follicles in response to chemokines. E. The principal function of mature dendritic cells is antigen capture.

A. Immature dendritic cells are ubiquitously present in skin and mucosal tissues.

The T cell receptor (TCR) complex differs from an immunoglobulin molecule in which one of the following ways? A. On average, a TCR binds antigen with much lower affinity than does an Ig molecule. B. The TCR can serve as a lymphocyte antigen receptor, but an Ig molecule cannot. C. Only the TCR can bind soluble antigen directly. D. The TCRs expressed by one clone of T cells can undergo changes in constant region structure after cellular activation, whereas Ig molecules expressed by one clone of B cells do not. E. The TCR polypeptide chains have short cytoplasmic tails and rely on associated proteins for signaling functions, whereas membrane Ig receptors are competent signaling molecules on their own.

A. On average, a TCR binds antigen with much lower affinity than does an Ig molecule.

A 67-year-old homeless man is brought to the emergency department after being found behind a neighborhood bar in freezing weather. On arrival, he has a shaking chill, fever, and cough productive of blood-tinged sputum. A chest radiograph shows lobar consolidations consistent with bacterial pneumonia. Blood cultures are positive for Streptococcus pneumoniae. Which of the following molecular patterns recognized by Toll-like receptors expressed on the surface of this patient's phagocytes is important for activating his innate immune system against this gram-positive bacterial infection? A. Peptidoglycan B. Double-stranded RNA C. Lipopolysaccharide (LPS) D. Lipoarabinomannan E. Phosphatidylinositol dimannoside

A. Peptidoglycan

Adaptive immune responses are slow to develop, taking days to weeks after exposure to reach their peak. However, these responses are more specific than innate responses, and also generate immunological memory. These latter features, which provide enhanced protection upon re-infection with the same pathogen, are the basis of: A. Vaccines B. Antibiotics C. Systemic shock D. Complement activation E. Phagocytosis

A. Vaccines

All of the following molecules are opsonins that facilitate efficient phagocytosis of microbes by neutrophils and macrophages EXCEPT: A. C3b B. C5a C. C-reactive protein D. IgG E. Mannose-binding lectin

B. C5a

Many of the inflammatory mediators produced by tissue macrophages at sites of infection act on the endothelial cells lining the blood vessel walls. An exception to this is (are) the: A. Cytokines that induce increased vascular permeability B. Chemokines that induce directed migration of blood monocytes C. Cytokines that induce increased expression of adhesion molecules D. TNF produced by tissue-resident sensor cells E. Bradykinin produced that causes pain

B. Chemokines that induce directed migration of blood monocytes

Which type of antigen-presenting cell is most important for activating naive T cells? A. Macrophage B. Dendritic cell C. Endothelial cell D. B lymphocyte E. Epithelial cell

B. Dendritic cell

Macrophages and neutrophils express several enzymes that are involved in biochemical mechanisms that kill ingested microbes. Which of the following is NOT an enzyme expressed by these cells? A. Inducible nitric oxide synthase (iNOS) B. Granzyme B C. Phagocyte oxidase D. Myeloperoxidase E. Lysozyme

B. Granzyme B

The antigen receptor on a T cell recognizes a degraded fragment of a protein (i.e., a peptide) bound to a specialized cell surface peptide-binding receptor called an MHC molecule. One key aspect of this system is that the peptides displayed on MHC molecules can be derived from intracellular proteins. This mode of antigen recognition is particularly important in allowing the adaptive immune response to detect infections by: A. Large helminthic parasites in the gastrointestinal tract B. Intracellular pathogens, such as viruses and some protozoa C. Extracellular bacteria that colonize the lungs D. Fungi that form hyphae in the bronchial airways E. Fungal infections in the skin epithelium

B. Intracellular pathogens, such as viruses and some protozoa

Some Pattern Recognition Receptors (PRRs) recognize nucleic acids, like RNA or DNA. Since our own cells contain human RNA and DNA, the activation of innate immune pathways by these PRRs must rely on additional criteria to discriminate self from nonself. Additional criteria include everything EXCEPT: A. The subcellular location of the RNA B. The presence of adenosine residues in viral RNA C. The methylation state of the DNA D. Unique structures found on viral RNA E. The subcellular location of the DNA

B. The presence of adenosine residues in viral RNA

A 15-year-old girl develops malaise, headache, and low-grade fever, followed by pharyngitis and cervical lymph node enlargement as a result of infectious mononucleosis caused by Epstein-Barr virus (EBV). Her acute symptoms resolve within 2 weeks, and the fatigue improves within 3 months. All of the following are required for CD8+ cytotoxic T lymphocyte (CTL) recognition and killing of EBV-infected cells EXCEPT: A. β2-Microglobulin B. HLA-A, -B or -C C. CD28 D. LFA-1 (leukocyte function-associated antigen-1) E. TAP (transporter associated with antigen processing)

C. CD28

CD8 is a protein that functions as a coreceptor for a subset of T cells and plays a significant role in all of the following EXCEPT: A. Recognition of peptide antigen bound to class I MHC molecules B. Maturation of MHC class I-restricted T cells C. Infection of T cells by human immunodeficiency virus (HIV) D. Signaling via Lck tyrosine kinase to initiate T cell activation E. Strengthening the binding of T cells to antigen-presenting cells, albeit with low affinity

C. Infection of T cells by human immunodeficiency virus (HIV)

In addition to T cells, which cell type is required for initiation of all T cell-mediated immune responses? A. Effector cells B. Memory cells C. Natural killer cells D. Antigen-presenting cells E. B lymphocytes

D. Antigen-presenting cells

Which of the following cell types is required for all humoral immune responses? A. Natural killer cells B. Dendritic cells C. Cytolytic T lymphocytes D. B lymphocytes E. Helper T lymphocytes

D. B lymphocytes

In patients with lymphomas, the cancer cells invade the bone marrow and destroy the environment required for normal hematopoiesis. This leads to bone marrow failure, which disrupts the production of hematopoietic cell lineages. All of the following cell types would be affected by this EXCEPT: A. Red blood cells B. Macrophages C. Lymphocytes D. Endothelial cells E. Granulocytes

D. Endothelial cells

Which of the following statements about the antigen-presenting function of macrophages is NOT correct? A. Macrophages are particularly important at presenting peptides derived from particulate or opsonized antigens that are internalized by phagocytosis. B. Macrophages become activated by the helper T cells to which they present microbial peptides, and as a result of this activation they become efficient at killing the microbes. C. Resting macrophages express low levels of class II MHC molecules, but higher class II MHC expression is induced on activation by the T cells to which they present antigen. D. Macrophages express highly variable, high-affinity receptors for many different antigens, and these receptors facilitate the internalization of the antigens for processing and presentation. E. Macrophages present antigen to T cells in lymphoid organs and many nonlymphoid organs.

D. Macrophages express highly variable, high-affinity receptors for many different antigens, and these receptors facilitate the internalization of the antigens for processing and presentation.

A 4-year-old girl stepped on a rusty nail in her backyard. Two days later, she is taken to the pediatrician because her heel is painful, red, and swollen and is warm to the touch. All of the following are mechanisms of innate immunity that may be protecting the patient against pathogenic microbes in the heel wound EXCEPT: A. Epithelial barrier function of the skin of her foot B. Intraepithelial lymphocytes present in the skin C. Circulating neutrophils migrating to the site of the wound D. Soluble cytokines that induce a local inflammatory response E. Circulating anti-tetanus toxin antibodies

E. Circulating anti-tetanus toxin antibodies

Which of the following is NOT a property shared by both CD4 and CD8? A. Binds to nonpolymorphic regions of MHC molecules B. Cytoplasmic tail associates with the Src family kinase Lck C. Is a member of the Ig superfamily D. Functions as a coreceptor for αβ TCRs E. Is expressed on the majority of mature blood T cells

E. Is expressed on the majority of mature blood T cells

In healthy adults, neutrophils represent approximately half of their white blood cells. During a bacterial infection, this number often rises to >80%. One factor contributing to this rise is: A. Recruitment of neutrophils from tissues into the blood B. Proliferation of neutrophils at the site of infection C. Proliferation of neutrophils in the blood D. Differentiation of blood monocytes into neutrophils E. Release of neutrophils into the blood from the bone marrow

E. Release of neutrophils into the blood from the bone marrow

Which one of the following molecules does NOT play an important role in the class II MHC pathway of antigen presentation? A. β2-Microglobulin B. Cathepsin C. Invariant chain D. HLA-DM E. Calnexin

A. B2-Microglobulin

In the class I MHC pathway of antigen presentation, peptides generated in the cytosol are translocated into the endoplasmic reticulum in which of the following ways? A. By ATP-dependent transport via the transporter associated with antigen-processing (TAP) 1/2 pump B. By passive diffusion C. By receptor-mediated endocytosis D. Through membrane pores E. Via the proteasome

A. By ATP-dependent transport via the transporter associated with antigen-processing (TAP) 1/2 pump

Neonates, elderly persons, and otherwise immunocompromised patients are particularly susceptible to infections with Listeria monocytogenes. These patients typically have fever and chills, often progressing to hypotension and septic shock. In healthy individuals, however, such intracellular microbes are usually effectively phagocytosed and killed by macrophages, which become activated via: A. CD40L-CD40 interactions between activated T helper cells and macrophages B. CD28-B7 interactions between activated T cells and macrophages C. Fas ligand-Fas interactions between activated cytotoxic T lymphocytes and macrophages D. TCR-MHC class II interactions between activated T helper cells and macrophages E. LFA-1-ICAM-1 interactions between activated T cells and macrophages

A. CD40L-CD40 interactions between activated T helper cells and macrophages

Many different NOD-like receptors, including several with pyrin domains and several with HIN domains, can function to trigger inflammasome assembly leading to the activation of caspase-1. The reason for many different sensors in this innate response system is that: A. Each NOD-like receptor is expressed in a different set of phagocytic cells, depending on its tissue location. B. Each NOD-like receptor resides in a different intracellular compartment. C. Each NOD-like receptor performs a different step in the multi-step cascade leading to inflammasome activation. D. Each NOD-like receptor binds to a different adapter protein and triggers a different form of the inflammasome. E. Each NOD-like receptor recognizes different PAMPs and is activated by different pathogens

A. Each NOD-like receptor is expressed in a different set of phagocytic cells, depending on its tissue location.

B cells express a complement receptor that binds to C3b cleavage products, such as iC3b and C3dg. When a B cell with an antigen receptor that specifically recognizes that pathogen also has its complement receptor stimulated because the pathogen is opsonized with these C3 fragments, B cell activation is greatly enhanced. Due to this mechanism, B cells can be activated by much lower concentrations of antigen (in this case, the pathogen) than if the antigen is devoid of complement components. This mechanism functions to: A. Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host B. Prevent B cells from being activated in response to antigens that are not pathogens C. Allow B cells to phagocytose the pathogen and help destroy it D. Induce increased rounds of B cell replication to make more pathogen-specific B cells E. Allow the B cell to block pathogen replication by interfering with multiple pathogen surface functions

A. Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host

The two major functional classes of effector T lymphocytes are: A. Helper T lymphocytes and cytotoxic T lymphocytes B. Natural killer cells and cytotoxic T lymphocytes C. Memory T cells and effector T cells D. Helper cells and antigen-presenting cells E. Cytotoxic T lymphocytes and target cells

A. Helper T lymphocytes and cytotoxic T lymphocytes

Which of the following is a unique property of the adaptive immune system? A. Highly diverse repertoire of specificities for antigens B. Self-nonself discrimination C. Recognition of microbial structures by both cell-associated and soluble receptors D. Protection against viral infections E. Responses that have the same kinetics and magnitude on repeated exposure to the same microbe

A. Highly diverse repertoire of specificities for antigens

When macrophages in a tissue encounter bacteria, they release cytokines that induce an inflammatory response. These cytokines act on other immune cells, to recruit them to the site of infection and to enhance their activities. In addition, these cytokines act on the endothelial cells of the blood vessel wall to: A. Increase their permeability, allowing fluid and proteins to leak into the tissue B. Solidify the tight junctions to prevent the bacteria from entering the blood C. Proliferate, allowing the blood vessel to enlarge D. Up-regulate microbicidal mechanisms, so they can kill bacteria E. Secrete anti-microbial peptides

A. Increase their permeability, allowing fluid and proteins to leak into the tissue

Chemokines such as CXCL8 have a key role in the rapid recruitment of neutrophils to the site in the tissue containing the focus of an infection. In this response, CXCL8 has two different functions. In addition to inducing integrin activation on the neutrophil, CXCL8 also functions to: A. Induce directional migration of the neutrophil in the tissue B. Induce increased expression of P-selectin and E-selectin on the endothelium C. Induce increased expression of integrins on the neutrophil surface D. Induce blood vessel dilation and fluid leakage into the infected tissue E. Induce increased phagocytic activity by the neutrophil

A. Induce directional migration of the neutrophil in the tissue

The strength of integrin-dependent binding of T cells to antigen-presenting cells (APCs) may be rapidly increased by which one of the following mechanisms? A. Integrin clustering and increased integrin affinity are induced by chemokines and antigen recognition. B. Integrins stored in cytoplasmic organelles are mobilized to the T cell surface in response to TCR-mediated signals. C. Integrin gene transcription is enhanced by chemokine-generated signals. D. The affinity of integrin ligands on APCs is increased in response to chemokines. E. Integrin ligands stored in cytoplasmic granules in the APCs are mobilized to the cell surface in response to CD40-CD40 ligand interaction.

A. Integrin clustering and increased integrin affinity are induced by chemokines and antigen recognition.

Secondary (or peripheral) lymphoid organs are sites for initiation of adaptive immune responses. Given the rarity of lymphocytes specific for any given antigen and the vast amount of body tissue that must be protected, the system of secondary lymphoid tissues is efficient because: A. It concentrates antigens in centralized locations for rare lymphocytes to encounter B. It provides the optimal environment for the rapid proliferation of lymphocytes C. It traps the pathogens and antigens in a contained environment so they cannot spread to other tissues in the body D. It helps the innate immune cells eliminate the infection by using lymphatic fluid to drain pathogens from the infected tissue E. It filters the lymph fluid and removes pathogenic organisms before they can enter the bloodstream

A. It concentrates antigens in centralized locations for rare lymphocytes to encounter

In a clinical trial of a new antiviral vaccine composed of a recombinant viral peptide and adjuvant, 4% of the healthy recipients did not show evidence of response to the immunization. Further investigation revealed that all the nonresponders expressed the same, single allelic variant of HLA-DR but all the responders were heterozygous for HLA-DR alleles. Which of the following is the most likely explanation for this finding? A. Response to the vaccine requires T cell recognition of complexes of the viral peptide with HLA-DR, but the peptide cannot bind to the allelic variant of HLA-DR found in the nonresponders. B. The nonresponders could not express class II MHC proteins. C. The viral peptide is not an immunodominant epitope. D. The nonresponders underwent determinant selection of another viral epitope. E. Because of technical errors, the nonresponders had not received adequate doses of the vaccine

A. Response to the vaccine requires T cell recognition of complexes of the viral peptide with HLA-DR, but the peptide cannot bind to the allelic variant of HLA-DR found in the nonresponders.

The pattern recognition receptors on cells of the innate immune system are genetically encoded, meaning that their sequences and specificities are determined prior to the development of the individual. In contrast, the antigen receptors of B and T lymphocytes arise from a random rearrangement process that occurs differently in each lymphocyte as it develops. One potential problem entailed by the random process that generates lymphocyte antigen receptors is the possibility that: A. Some antigen receptors might recognize the individuals on cells or antigens B. Many lymphocytes might generate antigen receptors that don't recognize anything C. Many lymphocytes might generate antigen receptors that recognize multiple different pathogens D. Some antigen receptors might recognize foreign tissues and lead to graft rejection during organ transplantation E. Some lymphocytes might not generate functional antigen receptor proteins

A. Some antigen receptors might recognize the individuals on cells or antigens

A vaccine administered in the autumn of one year may protect against the prevalent strain of influenza virus that originated in Hong Kong that same year, but it will not protect against another strain of influenza virus that originated in Russia. This phenomenon illustrates which property of the adaptive immune system? A. Specificity B. Amnesia C. Specialization D. Cultural diversity E. Self-tolerance

A. Specificity

A 4-year-old boy suffers from an immunodeficiency disease characterized by impaired T cell activation. The disease is caused by genetic deficiency of a membrane protein whose cytoplasmic tail is involved in intracellular signaling in response to T cell receptor (TCR) recognition of antigen. Which one of the following proteins does NOT fit this description? A. TCRα B. CD3γ C. ζ D. CD4 E. CD3ε

A. TCRα

The alternative pathway of complement activation has an important role in innate immunity, due to its ability to greatly amplify the amount of C3b deposited onto the pathogen surface. This amplification occurs because: A. The C3 convertase of the alternative pathway is much more active than those of the classical and lectin pathways. B. The C3 convertase of the alternative pathway works as a soluble enzyme in the plasma. C. The C3 convertase of the alternative pathway cannot be inactivated by complement regulatory factors in the host. D. The C3 convertase of the alternative pathway is more efficiently recruited to pathogen surfaces than the C3 convertases of the classical and lectin pathways. E. The C3 convertase of the alternative pathway contains C3b, and can generate more of itself.

A. The C3 convertase of the alternative pathway is much more active than those of the classical and lectin pathways.

One feature of Toll signaling that resembles the complement pathway is: A. The activation of an extracellular proteolytic cascade involving cleavage of self-proteins B. The deposition of Toll signaling proteins onto the microbial surface C. The release of soluble fragments of Toll that induce inflammation D. The assembly of a membrane attack complex in the microbial membrane following Toll activation E. The presence of receptors for Toll cleavage products on phagocytic cells to promote pathogen ingestion

A. The activation of an extracellular proteolytic cascade involving cleavage of self-proteins

The importance of complement activation as an innate immune defense against infections is illustrated by: A. The evolution of complement avoidance strategies by many pathogens B. The large number of proteins involved in the complement pathway C. The large number of complement regulatory pathways expressed by the host D. The existence of three different mechanisms for initiating complement activation E. The ability of the membrane attack complex to lyse some pathogens

A. The evolution of complement avoidance strategies by many pathogens

One surprising aspect of the immune system is that individuals make responses to human tissues from a different individual, causing serious problems for organ and tissue transplantation. The basis for this immune response is: A. The extensive polymorphism of MHC genes in the human population B. The fact that transplanted tissues often carry infectious microbes into the recipient C. The fact that individuals may differ in their blood group antigens (i.e., their blood type) D. The presence of many antigen-presenting-cells in the transplanted tissue E. The presence of many B and T lymphocytes in the transplanted tissue

A. The extensive polymorphism of MHC genes in the human population

Which of the following comparisons of the innate and adaptive immune systems is FALSE? A. The innate immune system is more likely to recognize normal self, and therefore cause autoimmunity, than is the adaptive immune system. B. Receptors used for recognition in innate immunity are encoded in the germline, whereas those of the adaptive immune system are encoded by genes generated via somatic recombination of germline receptor gene loci. C. The innate and adaptive immune systems share some of the same effector mechanisms. D. Both the innate and adaptive immune systems can recognize nonmicrobial substances. E. The innate immune system does not have memory but the adaptive immune system does.

A. The innate immune system is more likely to recognize normal self, and therefore cause autoimmunity, than is the adaptive immune system.

The majority of vaccines work by eliciting pathogen-specific antibodies that circulate in our bodies and protect us in the event that we are later exposed to that specific pathogen. For most viruses and bacterial toxins that we are vaccinated against, these pre-existing antibodies are protective because: A. They neutralize the virus or toxin, preventing it from attaching to and entering our cells. B. They bind to the virus or toxin and carry it to the liver where it can be degraded. C. They bind to the virus or toxin and directly induce lysis. D. They induce mucus production that helps flush the toxin or virus out of the body. E. They bind to epithelial cells and induce the production of antimicrobial peptides.

A. They neutralize the virus or toxin, preventing it from attaching to and entering our cells.

Although the complement cascade can be initiated by antibodies bound to the surface of a pathogen, complement activation is generally considered to be an innate immune response. This is because: A. Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces. B. When the complement cascade leads to the formation of a membrane-attack complex, the pathogen is killed. C. Several of the soluble products generated by complement activation lead promote the inflammatory response. D. Complement proteins bound to the pathogen promote uptake and destruction by phagocytic cells. E. The C3 convertase is only produced when complement activation is initiated by antibody binding to a pathogen.

A. Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces.

Vaccination against many infectious diseases has provided enormous benefit in developed countries, leading to the virtual eradication of diseases such as polio, measles, smallpox, and others. However, efforts to create long-lasting vaccines against some viral infections, like Influenza and HIV, have not been successful to date because: A. Viruses like HIV and Influenza undergo antigenic variation to evade previous immune responses. B. Viruses like HIV and Influenza spread too rapidly in the population for a vaccine to be effective. C. Viruses like HIV and Influenza have RNA, rather than DNA genomes, and are resistant to current vaccine strategies. D. Viruses like HIV and Influenza infect via mucosal surfaces, a route that is not well protected by current vaccine strategies. E. Viruses like HIV and Influenza are transmitted vertically (from mother to child) during fetal development, so babies are infected before they can be vaccinated

A. Viruses like HIV and Influenza undergo antigenic variation to evade previous immune responses.

Which one of the following comparisons between neutrophils and macrophages is true? A. Neutrophils that enter inflammatory sites can survive for days, but macrophages are very short lived and only survive for hours. B. Both neutrophils and macrophages are phagocytic and can kill internalized microbes. C. Neutrophils proliferate at inflammatory sites, but macrophages are terminally differentiated and cannot proliferate. D. Neutrophils, but not macrophages, express the high-affinity FcgRI receptor, which recognizes specific opsonins bound to microbes and facilitates phagocytosis. E. Both neutrophils and macrophages contain abundant cytoplasmic granules containing lysozyme, collagenase, and elastase.

B. Both neutrophils and macrophages are phagocytic and can kill internalized microbes.

CD1-restricted T cells differ from other T cells restricted to class I or class II MHC molecules in which one of the following ways? A. CD-1 restricted T cells cannot rapidly secrete cytokines. B. CD-1 restricted T cells recognize non-peptide antigens, such as lipids. C. CD-1 restricted T cells bind both cell-associated and soluble antigens. D. CD-1 restricted T cells express both CD4 and CD8 coreceptors. E. CD-1 restricted T cells are actually natural killer (NK) cells.

B. CD-1 restricted T cells recognize non-peptide antigens, such as lipids.

A healthy 45-year-old child-care worker becomes infected with a virus and develops a sore throat, cough, and fever. Infected cells in the bronchial mucosa of this patient process virus-encoded proteins through an intracellular pathway and display peptides derived from the protein on the cell surface bound to class I MHC molecules. CD8+ T cells migrate to the mucosa and recognize these peptide-MHC complexes. Which of the following components of the TCR actually bind to the viral peptide-MHC complex? A. Hypermutated regions: 1 in the α chain, 2 in the β chain B. Complementarity-determining regions: 3 in the α chain, 3 in the β chain C. Hypervariable regions: 2 in the α chain, 2 in the β chain D. Congenic regions: 1 in the α chain, 1 in the β chain E. One peptide-binding groove formed by the α chain and the β2-microglobulin chain

B. Complementarity-determining regions: 3 in the α chain, 3 in the β chain

CD44 expressed on the surface of T cells is critical for the binding of activated T cells to endothelium at sites of inflammation, and for the retention of T cells in extravascular tissues at sites of infection. CD44 does this by binding to which one of the following molecules? A. VCAM-1 B. Hyaluronate C. ICAM-1 D. Fibronectin E. E-selectin

B. Hyaluronate

After 2 years of hard work, a graduate student finally succeeds in creating a gene knockout mouse lacking CD4. The student is particularly careful to keep this mouse line in a microbe-free animal facility because these mice are expected to show: A. No ability to produce IgM antibodies B. Impaired ability to produce antibodies and activate macrophages C. No ability to activate naive class I-restricted T cells D. Complete absence of cytotoxic T lymphocyte (CTL) responses to viral infections E. Failure to produce neutrophils

B. Impaired ability to produce antibodies and activate macrophages

A young adult is exposed to a virus that infects and replicates in mucosal epithelial cells of the upper respiratory tract. One component of the protective immune response to this viral infection is mediated by CD8+ cytolytic T lymphocytes (CTLs), which recognize and kill virus-infected cells. The CTLs can recognize and kill the infected cells because: A. In response to interferon- secreted during the innate immune response to the virus, the mucosal epithelial cells express class II MHC, with bound viral peptides, on their cell surfaces. B. Mucosal epithelial cells, like all nucleated cells, express class I MHC molecules and are able to process cytoplasmic viral proteins and display complexes of class I MHC and bound viral peptides on their cell surfaces. C. Antibodies specific for viral antigens bind to these antigens on infected cell surfaces and engage Ig Fc receptors on the CTL, thereby targeting the CTL to the infected cells. D. Virus-infected mucosal epithelial cells migrate to draining lymphoid tissues, where they present viral peptide antigens to naive CD8+ T cells. E. Viral infection of the mucosal epithelial cells stimulates them to express E-selectin, which promotes CD8+ T cell adhesion.

B. Mucosal epithelial cells, like all nucleated cells, express class I MHC molecules and are able to process cytoplasmic viral proteins and display complexes of class I MHC and bound viral peptides on their cell surfaces.

The classical complement pathway is initiated by C1q binding to the surface of a pathogen. In some cases, C1q can directly bind the pathogen, for instance by recognizing proteins of bacterial cell walls, but in most cases C1q binds to IgM antibodies that are bound to the pathogen surface. How does this IgM-binding feature of C1q contribute to rapid, innate immune responses rather than to slow, adaptive responses? A. C1q induces B lymphocytes to begin secreting antibody within hours of pathogen exposure. B. Natural antibody that binds to many microbial pathogens is produced prior to pathogen exposure. C. C1q binds to C-reactive protein which then binds to IgM on the pathogen surface. D. C1q directly induces inflammation, recruiting phagocytes and antibodies from the blood into the infected tissue. E. C1q binds to dendritic cells in the infected tissue, inducing them to secrete inflammatory cytokines.

B. Natural antibody that binds to many microbial pathogens is produced prior to pathogen exposure.

A standard treatment of animal bite victims, when there is a possibility that the animal was infected with the rabies virus, is administration of human immunoglobulin preparations containing anti-rabies virus antibodies. Which type of immunity would be established by this treatment? A. Active humoral immunity B. Passive humoral immunity C. Active cell-mediated immunity D. Passive cell-mediated immunity E. Innate immunity

B. Passive humoral immunity

Epithelial surfaces provide the first line of defense against infection by the use of several types of mechanisms. One of the chemical mechanisms used by epithelia is: A. Joining of epithelial cells by tight junctions B. Secretion of antimicrobial peptides by epithelial cells C. Production of mucus, tears, or saliva in the nose, eyes, and oral cavity D. Movement of mucus by cilia E. Peristalsis in the gastrointestinal tract

B. Secretion of antimicrobial peptides by epithelial cells

Which one of the following statements about inhibitory receptors on natural killer (NK) cells is true? A. Inhibitory receptors on NK cells express ITAM motifs in their cytoplasmic tails. B. Some inhibitory receptors on NK cells recognize HLA-A or HLA-C. C. Some inhibitory receptors on NK cells are members of the integrin family. D. Some inhibitory receptors on NK cells are members of the Toll-like receptor family. E. Inhibitory receptors on NK cells are not expressed on the same NK cells that express activating receptors.

B. Some inhibitory receptors on NK cells recognize HLA-A or HLA-C.

Several subsets of innate lymphoid cells (ILCs) have been identified that share their patterns of cytokine production with the known subsets of T cells. The combined activity of related ILC and T cell subsets is effective in eradicating pathogenic infections because: A. ILCs cannot kill the pathogen, whereas the antigen-specific T cells can kill the pathogen. B. The early response of ILCs that reside at the site of infection is followed by the later more robust response of pathogen-specific T cells that migrate to the site of infection. C. The ILCs activate B cells to induce antibody responses whereas the T cells are able to directly eliminate the pathogen. D. The ILCs are induced to migrate from the site of infection to the draining lymph nodes where they activate the antigen-specific T cells. E. The ILCs are activated to secrete antimicrobial compounds which cause them to lyse, releasing RNA and DNA that act on T cells to stimulate T cell cytotoxic activities.

B. The early response of ILCs that reside at the site of infection is followed by the later more robust response of pathogen-specific T cells that migrate to the site of infection.

Inherited immunodeficiency diseases result from a single gene defect in one component of the immune system. By identifying the class of microbial pathogens a given immunodeficient individual becomes susceptible to, studies of these diseases indicate: A. Which type of antibiotics each patient should be given B. The essential immune mechanism required for resistance to each category of pathogen C. Whether the disease is a genetically inherited or an acquired form of immunodeficiency D. Whether the immunodeficiency disease is likely to be transmitted to another individual E. Whether the disease is likely to be life-threatening or not

B. The essential immune mechanism required for resistance to each category of pathogen

A previously healthy 8-year-old boy is infected with an upper respiratory tract virus for the first time. During the first few hours of infection, which one of the following events occurs? A. The adaptive immune system responds rapidly to the virus and keeps the viral infection under control. B. The innate immune system responds rapidly to the viral infection and keeps the viral infection under control. C. Passive immunity mediated by maternal antibodies limits the spread of infection. D. B and T lymphocytes recognize the virus and stimulate the innate immune response. E. The virus causes malignant transformation of respiratory mucosal epithelial cells, and the malignant cells are recognized by the adaptive immune system.

B. The innate immune system responds rapidly to the viral infection and keeps the viral infection under control.

A 43-year-old man with a history of kidney transplantation is on immunosuppressive drugs. He presents to the emergency department 84 days after transplantation with a slight fever, accompanied by violent shaking chills, rapid heart rate, and dangerously low blood pressure. Blood cultures are positive for gram-negative bacteria, including Klebsiella and Pseudomonas. Although the patient was initially alert and responsive to fluids and antibiotic therapy, his condition rapidly deteriorates into disseminated intravascular coagulation (DIC), hypoglycemia, and cardiovascular failure. Which of the following is an essential mediator of this patient's condition? A. Transforming growth factor-B B. Tumor necrosis factor-a C. Interleukin (IL)-2 D. IL-10 E. IL-3

B. Tumor necrosis factor-a

Multiple pathways for regulating complement activation limit the potential damage caused by complement deposition on host cells or caused by the spontaneous activation of complement proteins in the plasma. Genetic deficiencies in these mechanisms often lead to chronic inflammatory diseases, but in some cases can paradoxically lead to increased susceptibility to bacterial infections. This latter outcome may occur because: A. Complement regulatory proteins have dual functions in inhibiting and promoting complement activation. B. Uncontrolled complement activation leads to the depletion of serum complement proteins. C. The inhibition of the membrane attack complex by complement regulatory proteins normally leads to enhanced activation of the early steps of the complement pathway. D. Complement regulatory proteins normally cause the rapid depletion of plasma complement factors. E. Uncontrolled complement activation recruits the majority of phagocytic cells, leaving few remaining to fight infections in the tissues

B. Uncontrolled complement activation leads to the depletion of serum complement proteins.

γδ T cells may be important for recognition of common antigens at epithelial boundaries between the host and the external environment. The γδ T cells differ from the αβ T cells in which one of the following ways? A. γδ T cells recognize only nonprotein antigens. B. γδ T cells are not MHC-restricted and do not recognize MHC-associated antigens. C. The γδ TCR complex contains CD3γ or CD3δ but not CD3ε D. Most mature γδ T cells express either CD4 or CD8 but not both. E. γδ T cells lack key biologic activities, including the ability to lyse target cells.

B. γδ T cells are not MHC-restricted and do not recognize MHC-associated antigens.B. γδ T cells are not MHC-restricted and do not recognize MHC-associated antigens.

Which of the following is an example of how the innate immune response stimulates or modifies adaptive immunity? A. Tumor necrosis factor (TNF) secreted by helper T cells enhances adhesion molecules on endothelial cells and promotes recruitment of inflammatory cells. B. Interferon (IFN)-y produced by T helper cells is a potent activator of macrophages, allowing killing of phagocytosed microbes. C. B7-1 expression on antigen-presenting cells is up-regulated in response to signaling through Toll-like receptors, thus enabling costimulation of T cells. D. Infected cells coated by IgG3 are recognized by Fc receptors on natural killer cells, allowing efficient killing of the infected cells. E. Double-stranded RNA of replicating viruses potently stimulates IFN- expression by fibroblasts, inducing an "antiviral state" in neighboring, uninfected cells.

C. B7-1 expression on antigen-presenting cells is up-regulated in response to signaling through Toll-like receptors, thus enabling costimulation of T cells.

Both CD28 and CTLA-4 are receptors on T cells that are critical for regulating T cell activation. In which one of the following ways does CD28 differ from CTLA-4? A. Only CD28 binds the costimulatory ligands B7-1 and B7-2 expressed on professional antigen-presenting cells. B. CD28 counteracts positive, pro-proliferative T cell signals delivered by CTLA-4. C. CD28 is constitutively expressed on naive T cells, whereas CTLA-4 is expressed on activated T cells. D. CD28 binds its ligand with 10-fold greater affinity than does CTLA-4. E. CD28 is important for delivering "signal 1" for T cell activation, whereas CTLA-4 is important for delivering "signal"

C. CD28 is constitutively expressed on naive T cells, whereas CTLA-4 is expressed on activated T cells.

The principal function of the immune system is: A. Defense against cancer B. Repair of injured tissues C. Defense against microbial infections D. Prevention of inflammatory diseases E. Protection against environmental toxins

C. Defense against microbial infections

Antigen-presenting cells (APCs) perform which of the following functions in adaptive immune responses? A. Display major histocompatibility complex (MHC)-associated peptides on their cell surfaces for surveillance by B lymphocytes B. Initiate T cell responses by specifically recognizing and responding to foreign protein antigens C. Display MHC-associated peptides on their cell surfaces for surveillance by T lymphocytes D. Display polysaccharide antigens on their cell surfaces for surveillance by B lymphocytes E. Secrete peptides derived from protein antigens for binding to T cell antigen receptors

C. Display MHC-associated peptides on their cell surfaces for surveillance by T lymphocytes

During a humoral immune response to a newly encountered bacterial infection, B cells are first stimulated to proliferate and then secrete antibodies specific for the bacterium. The antibodies may then bind to the bacteria and facilitate ingestion of the microbes by phagocytic cells. In what phase of the humoral immune response does the binding of secreted antibodies to bacteria occur? A. Recognition phase B. Activation phase C. Effector phase D. Homeostatic phase E. Memory phase

C. Effector phase

Even when the complement cascade fails to proceed beyond generating the C3 convertase, complement activation is effective at inducing pathogen uptake and destruction. This process of immune protection is mediated by: A. Activation of complement inhibitory receptors on phagocytes that promote pathogen uptake B. Activation of soluble proteases in the serum that disrupt pathogen membranes C. Engagement of complement receptors on phagocytes by C3b and its cleavage products which promotes phagocytosis D. Engagement of complement receptors on B cells that promotes antibody production E. Stimulation of antimicrobial peptide secretion by phagocytes

C. Engagement of complement receptors on phagocytes by C3b and its cleavage products which promotes phagocytosis

Lymph nodes function as meeting points between antigen-bearing dendritic cells arriving from the tissue and recirculating B and T lymphocytes. Whereas the dendritic cells coming from the tissue enter the lymph node via the afferent lymphatic vessels, the recirculating lymphocytes enter the lymph node: A. Also from the lymph fluid draining the tissue B. Directly from their primary lymphoid organ where they develop C. From the blood by crossing the high endothelial venules D. By being trapped in the lymphoid follicle by resident macrophages E. By being carried there by dendritic cells

C. From the blood by crossing the high endothelial venules

Which of the following statements about the innate immune system is NOT true? A. Innate immunity is present in all multicellular organisms, including plants and insects. B. Deficiencies in innate immunity markedly increase host susceptibility to infection, even in the setting of an intact adaptive immune response. C. Innate immunity is better suited for eliminating virulent, resistant microbes than is adaptive immunity. D. The innate immune response can be divided into recognition, activation, and effector phases. E. The innate immune response against microbes influences the type of adaptive immune response that develops.

C. Innate immunity is better suited for eliminating virulent, resistant microbes than is adaptive immunity.

Unlike B lymphocytes, T lymphocytes do not generate a secreted form of their antigen receptor after they are activated and proliferate. This is because the effector functions of T cells are restricted to: A. Responses important in protozoan infections, but not other types of infections B. Interactions with large helminthic parasites, which cannot be phagocytosed C. Interactions with other cells, such as virus-infected cells or other immune cells D. Responses important in mucosal surfaces (e.g., the lung), where antibodies cannot go E. Stimulating B cells and not any other types of cells

C. Interactions with other cells, such as virus-infected cells or other immune cells

The required number of complexes of a microbial peptide and a particular class II MHC allele on the surface of an antigen-presenting cell to initiate a T cell response specific for the viral peptide is: A. At least equal to the number of complexes of self peptides with class II MHC on the cell surface B. Greater than 103 C. Less than or equal to 0.1% of the total number of class II MHC molecules on the cell surface D. Greater than 106 E. Zero

C. Less than or equal to 0.1% of the total number of class II MHC molecules on the cell surface

Which of the following statements best describes the "two-signal requirement" for naive lymphocyte activation? A. Lymphocytes must recognize two different antigens to become activated. B. Lymphocytes must recognize the same antigen at two sequential times to become activated. C. Lymphocytes must recognize antigen and respond to another signal generated by microbial infection to become activated. D. Both naive B and naive T lymphocytes must simultaneously recognize antigen for either to be activated. E. When lymphocytes recognize antigen, the antigen receptors must activate two-signal transduction pathways to become activated.

C. Lymphocytes must recognize antigen and respond to another signal generated by microbial infection to become activated.

NK cells can be activated following recognition of a virus-infected cell, if that cell has down-regulated expression of MHC class I proteins on its surface. However, NK cells can also recognize infected cells or tumor cells, even if they still express MHC class I proteins. In this latter case, activating receptors on NK cells are recognizing: A. Molecules on the target cell up-regulated by cellular or metabolic stress B. Cytokines secreted by the virus-infected or tumor cell C. MHC class I-like decoy molecules encoded by the virus D. Mutated self-proteins expressed by the tumor cell E. Double-stranded DNA in the cytoplasm of the infected or tumor cell

C. MHC class I-like decoy molecules encoded by the virus

Complement activation in the innate immune system can be initiated in the absence of antibody. Which of the following molecular components of the complement system is involved in initiation of antibody-independent complement activation? A. C1 B. C9 C. Mannose binding lectin D. CR2 E. Mannose receptor

C. Mannose binding lectin

The skin and bodily secretions provide the first line of defense against infection. One response in this category that is common during upper respiratory virus infections is: A. Production of antibodies B. Infiltration by white blood cells C. Mucus production D. Increased saliva production E. Fever

C. Mucus production

Which of the following is the main criterion that determines whether a protein is processed and presented via the class I MHC pathway in an antigen-presenting cell (APC)? A. Encoded by a viral gene B. Present in an acidic vesicular compartment of the APC C. Present in the cytosol of the APC D. Internalized into the cell from the extracellular space E. Small in size

C. Present in the cytosol of the APC

Selectins differ from integrins in which one of the following ways? A. Selectins are expressed only on endothelial cells and integrins are expressed only on leukocytes. B. Selectins are important mediators of leukocyte adhesion to endothelium, but integrins are not. C. Selectins bind carbohydrate ligands, but integrins do not. D. Selectins mediate rolling of leukocytes on endothelium, but integrins do not. E. Selectins are a family of homologous molecules, but integrins are not.

C. Selectins bind carbohydrate ligands, but integrins do not.

The first pattern recognition receptor (PRR) important in innate immune responses was discovered in the fruit fly Drosophila melanogaster. Stimulation of this receptor, called Toll, induces: A. The synthesis of prostaglandins and leukotrienes B. The inflammatory response in Drosophila hemolymph vessels C. The production of antimicrobial peptides D. The recruitment of phagocytic cells to the site of infection E. The activation of Drosophila complement

C. The production of antimicrobial peptides

The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by: A. The inability of active C3b to diffuse away in the blood plasma. B. The inability of active C3b to covalently attach to the membranes of eukaryotic cells. C. The rapid hydrolysis of active C3b in solution, rendering it inactive. D. The tight binding of active C3b to the C3 convertase. E. The ability of active C3b to recruit phagocytic cells.

C. The rapid hydrolysis of active C3b in solution, rendering it inactive.

Naive B and T lymphocytes are small, quiescent cells with little cytoplasm and low metabolic activity. Yet within hours after being activated following encounter with their antigen, these cells enlarge and up-regulate many biosynthetic and metabolic pathways. Approximately one day later, the cells begin dividing, and for several days they are the most rapidly dividing cells in the body, undergoing 2-4 rounds of cell division every day. In order to maintain this phenomenal rate of cell division, lymphoblasts must: A. Use the large energy stores accumulated by them when they were naive quiescent cells prior to their activation B. Engulf their neighboring small quiescent lymphocytes in order to take their lipids and proteins for raw material C. Up-regulate synthesis of mRNA and proteins, some of which encode for glucose transporters and enzymes used for glycolysis D. Phagocytose extracellular proteins and lipids and degrade them for energy production E. Macropinocytose metabolites and sugars from the blood for use in glycolysis

C. Up-regulate synthesis of mRNA and proteins, some of which encode for glucose transporters and enzymes used for glycolysis

Most normal tissues contain resident macrophages, and connective tissue sites in the gastrointestinal tract and the lung contain large numbers of these cells. Yet the blood also contains a high number of circulating 'classical' monocytes that can differentiate into macrophages after entering tissues. These circulating monocytes function to: A. Phagocytose and kill pathogens in the blood B. Line the endothelial surfaces of the blood vessels with phagocytic cells C. Enter lymph nodes and patrol for infecting microbes in these organs D. Amplify the local innate immune response by entering tissues that are infected E. Differentiate into dendritic cells during an inflammatory response

D. Amplify the local innate immune response by entering tissues that are infected

LFA-1 is an integrin that promotes T cell activation by which one of the following mechanisms? A. Binds to the α3 domain of class I MHC molecules, mediating high avidity between T cells and antigen-presenting cells (APCs) B. Binds to B7-1 or B7-2 on the surface of APCs, mediating "signal 2" C. Binds to GlyCAM-1 on high endothelial venules of lymph nodes, mediating rolling of T cells on endothelium D. Binds to ICAM-1 on the surface of a variety of cells, mediating firm adhesion between T cells and APCs or endothelial cells E. Binds to VCAM-1 on the surface of cytokine-activated endothelial cells, mediating homing of T cells to peripheral sites of inflammation

D. Binds to ICAM-1 on the surface of a variety of cells, mediating firm adhesion between T cells and APCs or endothelial cells

A 15-year-old girl develops malaise, headache, and low-grade fever, followed by pharyngitis and cervical lymph node enlargement as a result of infectious mononucleosis caused by Epstein-Barr virus (EBV). Her acute symptoms resolve within 2 weeks, and the fatigue improves within 3 months. Following the primary infection described in this patient, the patient's subsequent exposure to Epstein-Barr virus (EBV) will trigger clonal expansion of EBV-specific T cells expressing which one of the following surface molecules? A. CD62Lhigh B. CD44low C. CD45RAhigh D. CD45ROhigh E. CD21high

D. CD45ROhigh

Naive CD8+ T cells require signals in addition to T cell receptor recognition of peptide-MHC to become activated and differentiate into cytolytic T cells. These signals are called costimulatory signals and are provided by professional antigen-presenting cells (APCs), such as dendritic cells. If a virus infects epithelial cells in the respiratory tract but does not infect professional APCs, what process ensures that naive T cells specific for viral antigens will become activated? A. Cross-reactivity, whereby the naive CD8+ T cell recognizes a self antigen that is structurally similar to a viral antigen presented by dendritic cells B. Crossover, whereby part of the viral genome is exchanged with part of one chromosome of the host C. Crosstalk, whereby signals generated by the virus binding to class I MHC molecules intersect with T cell receptor signaling pathways D. Cross-presentation, whereby infected epithelial cells are captured by dendritic cells, and the viral proteins originally synthesized in the epithelial cells are processed and presented in association with class I MHC molecules on the dendritic cell E. Cross-dressing, whereby viral infection of the epithelial cell stimulates the expression of surface molecules that are typically found only on dendritic cells

D. Cross-presentation, whereby infected epithelial cells are captured by dendritic cells, and the viral proteins originally synthesized in the epithelial cells are processed and presented in association with class I MHC molecules on the dendritic cell

One form of anemia results when individuals have a deficiency in the enzyme phosphatidylinositol glycan A (PIGA). This enzyme is required for the membrane attachment of proteins anchored by glycolipids to the plasma membrane, using what is called a 'GPI-linkage.' Included in the group of GPI-linked cell surface proteins is DAF/CD55. These individuals become anemic because: A. DAF/CD55 prevents the lysis of red blood cells by infecting pathogens. B. DAF/CD55 normally prevents the spleen from clearing healthy red blood cells from the circulation. C. In the absence of PIGA, the red blood cell membrane is bare of proteins allowing increased access of complement activating proteins to attach to the cell membrane. D. DAF/CD55 is a complement inhibitory protein that inactivates any C3 convertase that may form on host cell surfaces. E. In the absence of PIGA, red blood cells are unable to synthesize high levels of hemoglobin.

D. DAF/CD55 is a complement inhibitory protein that inactivates any C3 convertase that may form on host cell surfaces.

A child who suffers from a persistent viral infection is found to have a deficiency in lymphocyte production and very few T and B cells. Other bone marrow-derived cells are produced in normal numbers, and MHC molecule expression on cells appears normal. Transfusion of mature T cells from an unrelated donor who had recovered from a previous infection by the same virus would not be expected to help the child clear his infection. Which one of the following is a reasonable explanation for why this therapeutic approach would fail? A. Viral infections are cleared by antibodies, not T cells. B. The patient's own immune system would destroy the transfused T cells before they could respond to the viral infection. C. T cells recognize peptides, not viral particles. D. Donor T cell viral antigen recognition is restricted by MHC molecules not expressed in the patient. E. In responding to the previous infection, the donor would have used up all his T cells specific for that virus.

D. Donor T cell viral antigen recognition is restricted by MHC molecules not expressed in the patient.

Antibodies and T lymphocytes are the respective mediators of which two types of immunity? A. Innate and adaptive B. Passive and active C. Specific and nonspecific D. Humoral and cell-mediated E. Adult and neonatal

D. Humoral and cell-mediated

Which of the following best describes clonal expansion in adaptive immune responses? A. Increased number of different lymphocyte clones, each clone specific for a different antigen during the course of an infection B. Increased number of different lymphocyte clones, each clone specific for a different antigen during development of the immune system, before exposure to antigen C. Increased number of lymphocytes with identical specificities, all derived from a single lymphocyte due to nonspecific stimuli from the innate immune system D. Increased number of lymphocytes with identical specificities, all derived from a single lymphocyte stimulated by a single antigen E. Increased size of the lymphocytes of a single clone due to antigen-induced activation of the cells

D. Increased number of lymphocytes with identical specificities, all derived from a single lymphocyte stimulated by a single antigen

The T cell receptor (TCR) complex contains: A. A highly variable antigen coreceptor B. CD28 C. Three homologous CD3 chains, each covalently linked to the TCR αβ heterodimer D. Invariable ζ (zeta) chains noncovalently linked to the TCR αβ heterodimer E. Igβ

D. Invariable zeta chains noncovalently linked to the TCR aβ heterodimer

Which of the following is a receptor on macrophages that is specific for a structure produced by bacteria but not by mammalian cells? A. CD36 (scavenger receptor) B. Fc receptor C. Complement receptor D. Mannose receptor E. ICAM-1

D. Mannose receptor

At 15 months of age, a child received a measles-mumps-rubella vaccine (MMR). At age 22, she is living with a family in Mexico that has not been vaccinated and she is exposed to measles. Despite the exposure, she does not become infected. Which of the following properties of the adaptive immune system is best illustrated by this scenario? A. Specificity B. Diversity C. Specialization D. Memory E. Nonreactivity to self

D. Memory

The mucosal tissues of the body have their own unique set of immune structures that function as sites for initiating adaptive immune responses. The necessity for mucosa-associated lymphoid tissues to have unique cell types (M cells) and structures is because: A. The mucous layer lining mucosal surfaces makes it difficult for normal antigen-presenting cells to function. B. The epithelial surfaces that line the gut, lungs, and nasal passages prevent antigen-presenting cells from accessing microbes and microbial products. C. The epithelial cells found in mucosal tissues are distinct from those that provide barrier functions to the skin. D. Mucosal sites, where most pathogens access the body, are exposed to vast numbers of diverse microbes. E. Mucosal tissues lack innate sensor cells that can respond to PAMPs and provide short-term innate immune protection

D. Mucosal sites, where most pathogens access the body, are exposed to vast numbers of diverse microbes.

The signaling pathways triggered by Toll-like receptors typically result in activation of which of the following pairs of transcription factors? A. NFAT and T-bet B. AP-1 and GATA-3 C. Fos and STAT-6 D. NFkB and AP-1 E. Lck and Jun

D. NFkB and AP-1

Mycobacteria are intracellular pathogens that have adapted to life inside phagocytic cells, such as macrophages. These intracellular bacteria are taken up by phagocytosis, similar to other pathogens, but the bacteria are not killed. One possible mechanism that could account for this immune evasion by mycobacteria is their ability to: A. Prevent induction of nitric oxide production in the phagosome B. Prevent the acidification of phagosomes C. Prevent the expression of antimicrobial peptides in the phagosome D. Prevent fusion of phagosomes with lysosomes E. Kill the macrophage before it kills them

D. Prevent fusion of phagosomes with lysosomes

A 3-year-old boy, who is small for his age, has a history of pyogenic (pus-producing) infections and cutaneous skin abscesses. Physical examination is remarkable for high fever, enlarged liver and spleen, and swollen cervical lymph nodes. A culture from an abscess on his arm reveals Staphylococcus aureus, a gram-positive bacteria that is also catalase-positive. Immunoglobulin and complement levels are normal. Results of the nitroblue tetrazolium test are consistent with a diagnosis of chronic granulomatous disease (CGD). The boy's immunodeficiency involves impaired generation of which of the following? A. C5a B. C-reactive protein C. Mannose-binding lectin D. Reactive oxygen intermediates E. Membrane attack complex

D. Reactive oxygen intermediates

Which one of the following statements about T cell tolerance to self proteins is accurate? A. Self proteins are not presented by the class I pathway because only microbial proteins, and not self proteins, are ubiquinated in the cytosol. B. Peptides derived from self proteins are not presented by the class I or class II pathways because MHC molecules are expressed only in response to infections. C. Self proteins are not presented by the class II pathway because endosomal acidic proteases digest microbial proteins but not eukaryotic proteins. D. Self peptide/self MHC complexes are formed and displayed by antigen-presenting cells in both class I and class II MHC pathways, but T cells that recognize these complexes usually are not present or are functionally inactive. E. Peptides derived from self proteins are not displayed by MHC molecules because they usually are displaced by the more abundant microbial peptides.

D. Self peptide/self MHC complexes are formed and displayed by antigen-presenting cells in both class I and class II MHC pathways, but T cells that recognize these complexes usually are not present or are functionally inactive.

In recent years, several new vaccines have been developed that are made from purified viral surface proteins, rather than intact or live viruses. They are referred to as subunit vaccines. In order to generate a protective adaptive immune response to a subunit vaccine, the viral protein(s) must be mixed with an adjuvant. The adjuvant functions to: A. Mimic the process of normal virus entry by binding to the host receptor and inducing receptor-mediated endocytosis B. Induce vascular permeability to promote the accumulation of fluid and serum proteins at the vaccine injection site C. Induce the production of chemotactic proteins that recruit neutrophils and then monocytes to the site of vaccine injection D. Stimulate dendritic cells to up-regulate co-stimulatory molecules and migrate to the regional lymph node E. Promote the activation of the complement cascade to induce complement deposition on the viral subunit proteins

D. Stimulate dendritic cells to up-regulate co-stimulatory molecules and migrate to the regional lymph node

Maturing dendritic cells that migrate to a lymph node from peripheral tissues end up mainly in: A. Follicles B. High endothelial venules C. The medullary sinus D. T cell zones E. Efferent arterioles

D. T cell zones

An infant with recurrent bacterial and fungal infections is suspected to have an immunodeficiency disease. Within two days after exposure to a pathogen, the organisms have proliferated to dangerous levels requiring immediate systemic antibiotic treatment. It is unlikely that this infant has a defect in B or T lymphocyte responses to the infection because: A. Bacteria and fungi do not require B cell or T cell responses for their clearance. B. Bacteria and fungi are not efficiently transported to draining lymph nodes to initiate adaptive immune responses. C. Systemic infections of bacteria and fungi are usually cleared by the spleen. D. The defective immune response occurs too rapidly following infection to be due to a defect in B or T lymphocytes responses. E. Adaptive immune responses require dendritic cells to take up and degrade pathogens.

D. The defective immune response occurs too rapidly following infection to be due to a defect in B or T lymphocytes responses.

Mannose binding lectins (MBL) and ficolins are the two classes of proteins that can initiate the lectin pathway of complement activation. These proteins are selective for activating complement on the surfaces of microbial pathogens rather than host cells because: A. Their higher-order oligomeric structure can be assembled only after the monomers first bind to pathogen membranes. B. They only recruit MASP (MBL-associated serine proteases) proteins when bound to pathogen surfaces and not when bound to host cells. C. They only undergo the conformational change needed to activate MASP proteins when bound to a pathogen and not when bound to a host cell. D. They only bind to carbohydrate side chains and oligosaccharide modifications found on pathogen surfaces but not on host cell membranes. E. The activated MASP proteins are rapidly inactivated by hydrolysis when present on the surface of a host cell

D. They only bind to carbohydrate side chains and oligosaccharide modifications found on pathogen surfaces but not on host cell membranes.

n the class I MHC pathway of antigen presentation, cytoplasmic proteins are tagged for proteolytic degradation by covalent linkage with which of the following molecules? A. Calreticulin B. Nuclear factor (NF)-kB C. Tapasin D. Ubiquitin E. Calnexin

D. Ubiquitin

Toll-like receptors (TLRs) are a family of homologous receptors expressed on many cell types and are involved in innate immune responses. Ten different mammalian TLRs have been identified, and several ligands for many of these receptors are known. Which of the following is a TLR ligand? A. Single-stranded RNA B. Transfer RNA C. Double-stranded DNA D. Unmethylated CpG DNA E. Heterochromati

D. Unmethylated CpG DNA

Many vaccines now in development will include highly purified, recombinant, or synthetic peptide antigens. These vaccine antigens are expected to stimulate highly specific immune responses, but they are less immunogenic than vaccines containing intact killed or live microbes. Adjuvants are substances added to such vaccines to enhance their ability to elicit T cell immune responses. Which of the following statements about adjuvants is NOT correct? A. Adjuvants induce local inflammation, thereby increasing the number of antigen-presenting cells (APCs) at the site of immunization. B. Adjuvants stimulate the expression of costimulators on local APCs. C. Adjuvants enhance local production of cytokines that promote T cell activation. D. Adjuvants prolong the expression of peptide-MHC complexes on the surface of APCs. E. Adjuvants bind to T cell antigen receptors and promote their proliferation.

E. Adjuvants bind to T cell antigen receptors and promote their proliferation.

Toll-like receptors and other receptors are potent activators of various components of the innate immune system. All of the following proteins are expressed in response to signaling by these receptors EXCEPT: A. Interleukin-12 B. E-selectin C. Tumor necrosis factor D. Inducible nitric oxide synthase (iNOS) E. CD28

E. CD28

An infection in the skin, such as a pimple, often produces pus. The major component of pus is: A. Toxic oxygen molecules released by macrophages B. Toxic nitrogen molecules released by macrophages C. NETs released by neutrophils D. Dead epithelial cells killed by lysozyme E. Dead and dying neutrophils

E. Dead and dying neutrophils

The production of antimicrobial peptides is one of the most evolutionarily ancient mechanisms of defense for multicellular organisms, and most eukaryotic species make many different forms of these proteins. For instance, human paneth cells in the gastrointestinal epithelium make 21 different defensins. The reason for this diversity of antimicrobial peptides is: A. Epithelial cells make different forms than those made by neutrophils. B. Neutrophils make many different defensins and store them as inactive proteins in their secretory granules. C. Most of them are produced only in response to infection. D. The production of different peptides is induced following a bacterial infection versus a fungal infection. E. Each one has distinct activities against Gram-negative bacteria, Gram-positive bacteria, or fungi.

E. Each one has distinct activities against Gram-negative bacteria, Gram-positive bacteria, or fungi.

A 4-year-old-girl sees her physician because of a severe necrotizing, oropharyngeal herpes simplex viral (HSV) infection. She has a past medical history of cytomegalovirus (CMV) pneumonitis and cutaneous HSV infection. Phenotypic analysis of her blood cells shows an absence of CD56+ and CD16+ cells. There are normal numbers of CD4+ and CD8+ cells in the blood, and serum antibody titers are normal. The patient's CD8+ T cells were able to kill virally infected target cells in vitro. Which of the following is NOT characteristic of this girl's immunodeficiency disease? A. Lack of cells whose activation is normally inhibited by self class I major histocompatibility complex (MHC) B. Impaired granzyme B-dependent killing of virally infected target cells C. Lack of cells that are activated by IL-15 D. Impaired interferon (IFN)-y production during early phases of viral infection E. Failure to form viral peptide-class I MHC complexes

E. Failure to form viral peptide-class I MHC complexes

A key feature of TLR signaling is the ability to induce inflammatory cytokine gene expression extremely rapidly following TLR stimulation. This is accomplished by signaling pathways using several mechanisms to activate transcription factors that are already present in the cell prior to TLR stimulation, but are kept in an inactive state. These signaling pathways use all of the following mechanisms EXCEPT: A. Induced ubiquitination leading to protein degradation B. Induced ubiquitination inducing protein-protein interactions C. Induced phosphorylation leading to nuclear translocation D. Induced phosphorylation leading to kinase activation E. Induced phosphorylation preventing protein degradation

E. Induced phosphorylation preventing protein degradation

Many different viruses encode proteins that function to down-regulate MHC class I expression on host cells following infection with the virus. This immune evasion mechanism allows the virus to hide from CD8 T lymphocytes that normally detect virus-infected cells by using their T cell antigen receptor to recognize viral peptides bound to MHC class I proteins on the surface of the infected cell. To counteract this immune evasion strategy, NK cells have: A. Activating receptors that recognize MHC class I proteins B. A mechanism to secrete antiviral peptides C. Inhibitory receptors that recognize viral capsid proteins D. Activating receptors that recognize viral capsid proteins E. Inhibitory receptors that recognize MHC class I proteins

E. Inhibitory receptors that recognize MHC class I proteins

When complement proteins are covalently deposited onto the surface of a bacterium, this can sometimes lead to direct lysis of the bacterium. However, more commonly, the deposition of complement proteins onto the bacterial surface does not directly harm the bacterium. Instead, these complement proteins aid in bacterial elimination by: A. Recruiting antibodies to the bacterial surface, leading the antibody-dependent neutralization B. Providing a mechanism for phagocytes to use their Fc receptors to recognize and ingest the bacterium C. Cross-linking carbohydrate structures on the bacterial surface, thereby preventing the bacterium from replicating D. Stimulating B lymphocytes to produce more antibodies against the bacterium E. Providing a mechanism for phagocytes bearing complement receptors to recognize and ingest the bacterium

E. Providing a mechanism for phagocytes bearing complement receptors to recognize and ingest the bacterium

Women with urinary tract infections caused by E. coli are generally treated with a course of antibiotics. A common complication of the antibiotic treatment is the occurrence of a vaginal yeast infection caused by Candida albicans, an organism that is normally present in very low numbers in the human vaginal tract. This complication occurs because: A. The E. coli infection damages the reproductive epithelium, causing a breach in the tight junctions and allowing invasion by the Candida albicans. B. The E. coli infection induces adhesion molecule expression on the reproductive epithelium, allowing attachment of the yeast. C. The antibiotic treatment kills all strains of fungi present in the reproductive tract, except the Candida albicans. D. The E. coli infection causes gastrointestinal distress leading to diarrhea. E. The antibiotics kill many of the commensal organisms in the reproductive tract, allowing overgrowth of the fungus.

E. The antibiotics kill many of the commensal organisms in the reproductive tract, allowing overgrowth of the fungus.

Macrophages express multiple types of receptors on their surface that stimulate phagocytosis of microbes, leading to pathogen internalization and destruction. Many of these receptors, such as Dectin-1, rely on direct recognition of a PAMP on the pathogen surface. However, some receptors that stimulate phagocytosis rely on soluble factors (not associated with the phagocyte membrane) to identify and mark the pathogen for uptake by the phagocyte. One such receptor is: A. The mannose receptor B. The class A scavenger receptor C. The lipid receptor D. The macrophage C-type lectin receptor E. The complement receptor

E. The complement receptor

Which of the following statements is consistent with the process of clonal selection? A. The specificity of a lymphocyte antigen receptor changes to accommodate the structure of an antigen that binds to it. B. Many different antigen receptors with different specificities are expressed on each lymphocyte. C. Lymphocytes do not express antigen receptors on their cell surfaces until after exposure to antigen. D. The diversity of the lymphocyte repertoire for antigens is very small before exposure to antigen but increases significantly after antigen exposure. E. The diversity of the lymphocyte repertoire for antigens is very large before exposure to antigen, with millions of different clones of lymphocytes, each having a different specificity.

E. The diversity of the lymphocyte repertoire for antigens is very large before exposure to antigen, with millions of different clones of lymphocytes, each having a different specificity.

Individuals with defects in T cell development have a severe immunodeficiency disease called SCID (severe combined immunodeficiency disease). In these individuals, the absence of all T cells causes defects in both cell-mediated (T cell-based) and humoral (antibody-based) immune responses. The defect in antibody responses in SCID patients is due to: A. The important role of T cells in regulating B cell development in the bone marrow B. The inter-dependence of T cells and B cells for the normal development of secondary lymphoid organs. C. The absence of phagocytic cells needed for antibody-dependent pathogen clearance in SCID patients D. The poor survival of B cells in patients with defects in their T cells E. The important role of T follicular helper cells in generating protective antibody responses

E. The important role of T follicular helper cells in generating protective antibody responses

Stimulation of the nucleic acid sensing TLRs that reside in endosomal membranes induces the production of a different cytokine response than is produced by stimulation of the plasma membrane TLRs. In part, this distinction is based on the different adapter proteins used by the nucleic acid sensing TLRs, leading to the activation of IRF factors. The cytokine response following stimulation of nucleic acid-sensing TLRs is characterized by production of: A. The antiviral cytokine, type I interferon B. TNF-a, which induces increased vascular permeability C. Antimicrobial peptides by macrophages D. Chemokines that recruit neutrophils E. The inflammatory complement fragments, C3a and C5a

E. The inflammatory complement fragments, C3a and C5a

The terminal components of the complement pathway assemble to form a membrane attack complex that can induce pathogen lysis and death. Yet, evidence indicates that this feature of complement is less important than the earlier steps that promote pathogen opsonization and induce inflammation. This conclusion is based on: A. In vitro experiments showing that very few species of bacteria are susceptible to lysis by the membrane attack complex B. Experiments indicating that only bacteria, but not viruses or fungi, are susceptible to lysis by the membrane attack complex C. The very low levels of terminal complement components in the serum D. The fact that other mammalian species lack the terminal components of the complement pathway needed to form the membrane attack complex E. The limited susceptibility to infections of patients with deficiencies in terminal complement components

E. The limited susceptibility to infections of patients with deficiencies in terminal complement components

Given the enormous heterogeneity of antigen receptors expressed on the populations of naive B and T lymphocytes, the adaptive immune response relies on a process whereby the rare lymphocyte that binds to the antigen is first induced to proliferate, before it can perform its effector function. For B cells, there is a clever mechanism that ensures that the specificity of the antibody secreted by the plasma cell will recognize the same pathogen that initially stimulated the B cell antigen receptor and induced B cell proliferation. This mechanism is: A. The naive B cell expresses an array of different B cell antigen receptors, and randomly chooses which specificity of antibody to secrete as a plasma cell. B. The naive B cell expresses a single specificity of B cell antigen receptor, and then up-regulates the expression of this receptor so it can bind tightly to the pathogen. C. The plasma cell proliferates after it has finished secreting antibody to generate more plasma cells with specificity for the pathogen. D. The plasma cell traps secreted antibody molecules in its extracellular matrix and uses these antibodies to bind to the pathogen. E. The naive B cell expresses a membrane-bound form of the antibody as a receptor, and secretes that same antibody when it differentiates into a plasma cell.

E. The naive B cell expresses a membrane-bound form of the antibody as a receptor, and secretes that same antibody when it differentiates into a plasma cell.