Immunology exam 1

e

A term generally used to describe all white blood cells is _____. a. hematopoietic cells b. myeloid progenitor c. dendritic cells d. monocytes e. leukocytes.

Skin; mucosal epithelium of the gastrointestinal tract; mucosal epithelium of the respiratory tract; mucosal epithelium of the urinogenital tract.B. (i) Mechanical (physical) barriers. Tight junctions between the epithelial cells prevent the penetration of pathogens between the cells to underlying tissues. In addition, there is a flow of air and fluid over epithelial surfaces, which oxygenates and flushes the surface, preventing anaerobic bacterial growth and transient adhesion. On ciliated epithelial surfaces, such as those of the respiratory tract, the formation of a layer of mucus that is kept in continual movement by the beating cilia inhibits colonization and invasion by microorganisms. (ii) Chemical barriers. The epithelium produces a variety of chemical substances that interfere with the adherence of microorganisms to epithelium and with their replication. The skin produces fatty acids in sebaceous glands, whi

A.Name the parts of the body where epithelia act as barriers to infection. B. Describe the three main ways in which epithelia carry out this barrier function, giving details of the mechanisms employed.

a

All of the following acute-phase proteins increase in concentration in the plasma during inflammation with the exception of _____. a. albumin b. serum amyloid A protein c. fibrinogen d. C3 e. mannose-binding lectin.

d

All of the following are correct in reference to type I interferons except _____. a. Type I interferons inhibit the replication of viruses. b. In the presence of type I interferons, virus-infected cells undergo cell-surface changes that render them more susceptible to attack by NK cells. c. Not only can most cells synthesize type I interferons, but they can also respond to them. d. The receptor for type I interferons is abundant in the cytosol. e. Type I interferons function in autocrine and paracrine fashions. f. Type I interferons promote NK-cell proliferation and differentiation into cytotoxic cells.

b

All of the following are examples of chemical barriers of innate immunity except _____. a. lactic acid b. normal microbiota c. lysozyme d. fatty acids e. proteases.

a

All of the following complement proteins help form a pore in the pathogen's membrane except _____. a. C3b b. C5b c. C6 d. C7 e. C8 f. C9.

a

All of the following induce fever except _____. a. IL-12 b. IL-6 c. IL-1 d. TNF-\alpha.

a

All of the following statements are characteristic of secondary immune responses except _____. a. Secondary immune responses are activated when primary immune responses fail to completely eradicate an infection. b. Secondary immune responses are restricted to adaptive immune responses. c. Memory cells are activated rapidly during secondary immune responses. d. Secondary immune responses are orders of magnitude greater than primary immune responses. e. During a secondary immune response to a booster vaccine, it is possible to experience a primary immune response to an unrelated vaccine component encountered for the first time.

e

All of the following statements regarding Toll-like receptors are true except _____. a. They exist as either transmembrane homodimers or heterodimers. b. The extracellular domain detects the microbial component. c. They facilitate changes in gene expression. d. They sense molecules not found in or on human cells. e. The cytoplasmic signaling domain contains a variable number of leucine-rich repeat regions (LRRs).

A. The cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface is called complement fixation, and is the reaction on which the alternative, lectin, and classical pathways of complement activation converge. B. The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C4b2a), whereas the alternative pathway uses the alternative convertase (C3bBb). C. C3 is the most abundant complement component in the plasma and circulates as a zymogen, an inactive enzyme. When cleaved into C3a and C3b, three different effector mechanisms are armed: (1) C3b binds to and tags pathogens for destruction by phagocytes through binding to a C3b receptor, CR1; (2) C3b contributes to a multicomponent enzyme, C5 convertase, that catalyzes the assem

Although activation of the three different pathways of complement involves different components, the three pathways converge on a common enzymatic reaction referred to as complement fixation. A. Describe this reaction. B. Describe the enzyme responsible for this reaction in the alternative pathway. C. Identify the three effector mechanisms of complement that are enabled by this common pathway.

b

An adaptor protein in the inflammasome is required to link _____ to the NOD-like receptor NLRP3. a. MyD88 b. procaspase-1 c. RIPK2 d. TAKI e. IKK.

b

An example of an antimicrobial peptide that protects epithelial surfaces from pathogens is _____. a. glycoprotein b. defensin c. proteoglycan d. lysozyme e. sebum.

a

C-reactive protein binds to _____. a. phosphorylcholine b. mannose-containing carbohydrates c. lipoteichoic acid d. flagellin e. MASP-1/MASP-2.

C

C-type lectins are so called because of the role of _____ in facilitating receptor:ligand interactions. a. carbohydrate b. CR1 c. calcium d. chemokines e. caspases.

c

Damage to tissues triggers a cascade of plasma proteins involving bradykinin and is known as _____. a. the alternative pathway of complement b. the coagulation system c. the kinin system d. receptor-mediated endocytosis e. the acute-phase response.

The hallmarks of inflammation are heat, redness, pain, and swelling (edema). These are caused by a combination of vasodilation (causing redness and heat), increased vascular permeability and the consequent infiltration of fluid and leukocytes from the blood into the infected site (causing swelling, and also pain as a result of the increased pressure on local nerve endings).

Describe the characteristics commonly associated with inflammation and what causes them.

(i) Neutralization. By binding to the surface of a pathogen, antibodies interfere with the ability of the pathogen to grow and replicate. Antibody binding to a pathogen or a bacterial toxin can also inhibit its binding to receptors on host cells and therefore prevent its entry into cells. (ii) Opsonization. Antibody coating the surface of a pathogen or toxin can promote phagocytosis of the antibody-covered particle. Antibodies acting in this way are known as opsonins. The antibody-bound material interacts with Fc receptors on the surface of phagocytic cells such as macrophages and neutrophils, which bind the constant region (the stem) of the antibody. Stimulation of Fc receptors in this way stimulates the engulfment and degradation of antibody-coated material by the phagocyte. (iii) Complement activation. IgG or IgM antibody bound to a pathogen stimulates activation of the complement system, leading to the deposition

Describe three distinct mechanisms by which antibodies eradicate infection.

d

During an infection, _____ are mobilized in large numbers from the bone marrow. a. dendritic cells b. memory cells c. macrophages d. neutrophils e. B cells.

e

Effector cells that secrete antibodies are known as _____. a. natural killer cells b. cytotoxic T cells c. helper T cells d. M cells e. plasma cells f. regulatory T cells.

b

Examples of granulocytes include all of the following except: a. neutrophil b. monocyte c. basophil d. eosinophil. e. All of the above are examples of granulocytes.

e

Examples of pathogens that cause human disease include: a. bacteria b. viruses c. fungi d. parasites (protozoans and worms). e. All of the above are examples of pathogens that cause human disease.

A. Spontaneous hydrolysis of C3 without cleavage exposes its highly reactive thioester bond, forming iC3. Factor B binds to iC3, is cleaved by factor D, and consequently releases a small fragment called Ba. The larger fragment, Bb, remains associated with iC3 to form iC3Bb, a soluble C3 convertase, which cleaves C3 into C3a and C3b. The reactive thioester bond of C3b is attacked by R-OH and R-NH2 groups on the surface of the pathogen, where it becomes anchored and binds to factor B. Factor D then cleaves factor B, releasing fragment Ba and forming C3bBb on the pathogen surface. B. Factor P (properdin) binds to C3 convertase (C3bBb) bound to the pathogen surface, and inhibits the proteolytic degradation of C3bBb. This stabilizes the C3 convertase and enhances the rate of C3b deposition on the pathogen surface.

Explain how the alternative C3 convertase on pathogen cell surfaces is (A) formed and (B) stabilized.

G-protein-coupled receptors for the anaphylatoxins C3a and C5a are found on phagocytes, mast cells, and the endothelial cells of blood vessel walls. Anaphylatoxin bound to mast cells causes them to degranulate, releasing inflammatory mediators such as histamine and leading to increased vascular permeability. Through their action on endothelial cells, anaphylatoxins exert vasoactive effects on blood vessels, contributing to increased vascular permeability and increased blood flow, which facilitate the extravasation of plasma proteins, such as complement proteins and antibodies, and the recruitment of cells to infected tissues through increased adherence and chemotaxis. Phagocytic activity is enhanced by anaphylatoxins, which bring about increased levels of CR1 and CR3 and microbicidal activity. All these activities enhance inflammation.

Explain how the anaphylatoxins C3a and C5a contribute physiologically to inflammation during complement activation.

A. The cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface is called complement fixation, and is the reaction on which the alternative, lectin, and classical pathways of complement activation converge. B. The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C4b2a), whereas the alternative pathway uses the alternative convertase (C3bBb). C. C3 is the most abundant complement component in the plasma and circulates as a zymogen, an inactive enzyme. When cleaved into C3a and C3b, three different effector mechanisms are armed: (1) C3b binds to and tags pathogens for destruction by phagocytes through binding to a C3b receptor, CR1; (2) C3b contributes to a multicomponent enzyme, C5 convertase, that catalyzes the assem

Explain the steps that take place when a bacterium is opsonized via C3b:CR1 interaction between the bacterium and a resident macrophage in tissues.

C3 is a key element in the initiation of the complement cascade in all three pathways of complement activation, namely the alternative, lectin, and classical pathways. Its cleavage into C3a and C3b occurs early in the complement cascade. C3a acts as an inflammatory mediator and recruits inflammatory cells to the site of infection. C3b becomes fixed to the pathogen surface and facilitates the opsonization of pathogens by phagocytes and the assembly of complement components for perforation of the pathogen membrane. In the absence of C3, all three pathways of complement activation would be arrested and extracellular pathogens would escape immune detection until adaptive immune mechanisms develop fully many days later.

Explain why a genetic deficiency of C3 leads to a type of immunodeficiency characterized by recurrent and severe infections.

Antibiotics attack the microbiological barriers of intestinal epithelia. The normal microbiota sensitive to the antibiotics are killed off and the intestine can then be recolonized and overgrown by microorganisms that in normal circumstances are present in very small numbers and thus do not cause a problem. An example is a condition called pseudomembranous colitis caused by the overgrowth of Clostridium difficile. A membrane-like substance is produced in the large intestine, causing an obstruction that can block intestinal flow and usually requires surgical removal.

How can antibiotics upset the barrier function of intestinal epithelia? Give a specific example.

The four classes of pathogen are bacteria, viruses, fungi, and parasites (protozoa and worms). Examples of these pathogens are given in Figure 1.4.

Identify the four classes of pathogens that provoke immune responses in our bodies and give an example of each.

d

Identify the incorrectly paired molecular association. a. iC3: factor B b. CR4: iC3b c. properdin: C3bBb d. membrane cofactor protein: C3b2Bb e. decay-accelerating factor: C3bBb.

e

Immediately after engagement of NK-cell Toll-like receptors, the NK cell _____. a. discharges cytotoxic granules b. ligates IL-12R\beta1 and IL-12R\beta 2 c. synthesizes and secretes IL-15 d. synthesizes and secretes IL-12 e. synthesizes and secretes type I interferons.

b

In most cases, adaptive immune responses rely on the initial activation of _____ in secondary lymphoid tissue: a. macrophages b. T cells c. B cells d. dendritic cells e. epithelium.

C

Lectins recognize microbial _____. a. phosphate-containing lipoteichoic acids b. nucleic acids c. carbohydrates d. flagellin e. sulfated polysaccharides.

d, g

Macrophages bear on their surface receptors for all of the following except _____. (Select all that apply). a. mannose b. glucans c. C3b d. muramyl dipeptide e. lipopolysaccharide f. lipoteichoic acid g. CpG-rich bacterial DNA.

a2, b3, c1

Match the condition/disease in column A with its description in column B. Use each answer only once. Column A ___a. X-linked hypohidrotic ectodermal dysplasia and immunodeficiency (NEMO deficiency) ___b. septic shock ___c. chronic granulomatous disease Column B 1. insufficient superoxide production in neutrophils compromises the respiratory burst 2. failure to translocate NF\kappaB and activate macrophages due to deficiency in IKK\gamma subunit 3. allelic polymorphism of TLR4 with glycine at position 299 causing reduced responsiveness to LPS of Gram-negative bacteria

a3, b6, c12345, d12345. e7, f5, g8, h9

Match the innate immune receptor in column A with its ligand(s) in column B. More than one ligand may be used for each immune receptor. Column A ___a. lectin receptor ___b. scavenger receptor ___c. CR3 ___d. CR4 ___e. CR1 ___f. TLR4:TLR4 ___g. TLR5 ___h. TLR3 Column B 1. iC3b 2. lipophosphoglycan 3. carbohydrates (for example mannose or glucan) 4. filamentous hemagglutinin 5. lipopolysaccharide (LPS) 6. negatively charged ligands (for example sulfated polysaccharides and nucleic acids) 7. C3b 8. flagellin 9. RNA

a2, b4, c5, d3, e1

Match the term in column A with its description in column B. Column A ___a. interferon response ___b. apoptosis ___c. extravasation ___d. respiratory burst ___e. acute-phase response Column B 1. a notable rise or reduction of plasma proteins in response to IL-6 2. stimulates inhibition of viral replication 3. temporary rise in oxygen consumption and toxic oxygen species production 4. cellular suicide characterized by DNA fragmentation 5. migration of neutrophils into inflamed tissues

a1, b3, c5, d4, e2

Match the term in column A with its description in column B. Column A Column B ___a. oligoadenylate synthetase ___b. plasmacytoid dendritic cell (PDC) ___c. RIG-I-like helicase ___d. protein kinase R (PKR) ___e. NK-cell synapse 1. activates endoribonucleases that degrade viral RNA 2. facilitates adhesion and information exchange between cells undergoing surveillance via activating and inhibitory receptors 3. synthesizes 1000 times more interferon than do other cells 4. inhibits protein synthesis by phosphorylating eIF-2 5. contains domains that bind to viral RNA and mitochondrial-associated adaptor proteins

a, i

NK cells express all of the following proteins either on endosome membranes or on their cell surface with the exception of _____. (Select all that apply) a. CD3 b. type I interferon receptor c. CR3 d. CD56 e. LFA-1 f. activating receptors g. inhibitory receptors h. TLR3 i. TLR4 j. IL-12R\beta1 and IL-12R\beta2.

b

Of the following Toll-like receptors, which is the most highly conserved and displays the smallest amount of allelic polymorphism? a. TLR1 b. TLR8 c. TLR10 d. TLR6 e. TLR4.

c, d

On the basis of laboratory experiments, a possible scenario for the activation of an adaptive immune response would involve _____ within an infected tissue. (Select all that apply.) a. a balanced number of myeloid dendritic cells and NK cells b. an abundance of NK cells compared with myeloid dendritic cells c. a shortage of NK cells compared with myeloid dendritic cells d. migration of myeloid dendritic cells to secondary lymphoid tissue e. migration of NK cells to secondary lymphoid tissue.

TLR-4, TLR1:TLR2, and TLR2:TLR6 are transmembrane receptors anchored on the plasma membrane surface of human cells and interact with pathogens located in extracellular locations. In contrast, TLR3, 7, 8, and 9 are anchored in endosomal membranes located in the cytosol, where the intracellular degradation of pathogens takes place.

Other than their ligand specificity, what is a key difference between TLR5, TLR4, TLR1:TLR2, and TLR2:TLR6 compared to TLRs 3, 7, 8, and 9?

The cytokines released by activated macrophages have three principal effects. Some cytokines act as chemoattractants and recruit other leukocytes into the infected tissue, for example neutrophils, which efficiently phagocytose and kill bacteria, forming pus. Other cytokines act on the endothelial cells of local blood vessels to increase vascular permeability and vasodilation, thus initiating inflammation of the infected tissue.

Phagocytosis of either microbes or microbial constituents by macrophages is followed by the activation of macrophages and the secretion of cytokines. What are the main effects of these molecules?

b, e

Plasmacytoid dendritic cells _____. (Select all that apply.) a. detect viral infection by using TLR4 b. produce large amounts of the type I interferons when activated c. are found exclusively in the blood d. make up 10% of circulating leukocytes e. have a cytoplasmic morphology resembling that of antibody-producing plasma cells.

A. The cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface is called complement fixation, and is the reaction on which the alternative, lectin, and classical pathways of complement activation converge. B. The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C4b2a), whereas the alternative pathway uses the alternative convertase (C3bBb). C. C3 is the most abundant complement component in the plasma and circulates as a zymogen, an inactive enzyme. When cleaved into C3a and C3b, three different effector mechanisms are armed: (1) C3b binds to and tags pathogens for destruction by phagocytes through binding to a C3b receptor, CR1; (2) C3b contributes to a multicomponent enzyme, C5 convertase, that catalyzes the assem

Review the differences between the three pathways of complement (alternative, lectin, and classical) in terms of how they are activated. B. Distinguish which pathway(s) are considered part of an adaptive immune response and which are considered part of innate immunity, and say why.

c

Scavenger receptor SR-B recognizes _____. a. lipopolysaccharides b. teichoic acid c. filamentous hemagglutinin d. CpG-rich bacterial DNA e. lipids.

a, c, d, f

Soluble effector molecules are effective when encountering pathogens in/on _____. (Select all that apply.) a. extracellular spaces b. cytoplasm c. epithelial surfaces d. interstitial spaces e. vesicular compartments f. lymph.

b

Spherical regions in lymph nodes containing areas that are packed densely with proliferating B cells are called _____. a. efferent vessels b. germinal centers c. red pulp zones d. periarterial lymphoid sheaths e. medullary sinuses.

b

Stimulation of NK cells by IL-12 _____. a. enhances their cytotoxic potential b. skews their differentiation into effector NK cells c. induces the synthesis and secretion of IL-15 by NK cells d. turns off type I interferon production by NK cells e. induces the NK cell to undergo programmed cell death.

c

The C3 convertase that functions in the lectin pathway of complement activation consists of _____. a. C3bBb b. C3b2a c. C4b2a d. C4b2b e. C3b2Bb.

a

The _____ is (are) the lymphoid organ(s) that filter(s) the blood. a. spleen b. tonsils c. Peyer's patches d. appendix e. adenoids.

innate immunity

The first line of defense against microorganisms that infect the body is referred to as _____.

c

The following cytokines activate NK cells early in the course of a viral infection with the exception of _____. a. IFN-\alpha b. IFN-\beta c. IFN-\gamma d. IL-12 e. IL-15.

b

The function of uterine NK cells (uNK) is to _____. a. kill virus-infected cells b. secrete growth factors that promote blood vessel growth to supply the placenta c. activate resident macrophages by secreting inflammatory cytokines d. secrete 1000 times more type I interferon than other cells to protect the fetus from viral infection.

b

The importance of CD59 (also known as protectin) is to _____. a. promote the speed of complement activation by protecting C3 convertase C3bBb from proteolytic degradation b. prevent the recruitment of C9 c. dissociate the components of the alternative C3 convertase d. prevent the attachment of C3b to host cell surfaces e. inhibit the anchoring of C5b, C6, and C7 to host cell surfaces.

e

The ligands of endosomal Toll-like receptors are _____. a. lipids of Gram-negative bacteria b. flagellin proteins of bacteria c. lipids of Gram-positive bacteria d. zymosan of fungi e. nucleic acids of viruses and bacteria.

e

The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are _____. a. factor B and factor H b. factor H and factor I c. factor B and factor I d. decay-accelerating factor and factor H e. decay-accelerating factor and membrane cofactor protein.

c

The most abundant type of leukocyte in human peripheral blood is the _____. a. eosinophil b. basophil c. neutrophil d. monocyte e. lymphocyte.

17 a

The name given to cytokines that recruit cells to move towards areas of inflammation is _____. a. chemokines b. caspase-recruitment domains (CARDs) c. inflammakines d. adhesion molecules e. pyrogens.

b

The pH of the phagosome increases following phagocytosis because _____. a. the microbe delivers a significant number of hydroxyl ions in its cytosol that are released upon membrane disruption b. hydrogen ions are eliminated by the activity of NADPH oxidase and superoxide dismutase c. azurophilic granules deliver alkaline substances d. catalase consumes hydrogen ions once activated.

c

The progenitors of macrophages are _____. a. megakaryocytes b. dendritic cells c. monocytes d. neutrophils e. erythrocytes f. M cells.

e

The spleen differs from other secondary lymphoid organs in which of the following ways? a. It does not contain T cells. b. It filters blood as well as lymph. c. It is populated by specialized cells called M cells. d. It receives pathogens via afferent lymphatic vessels. e. It has no connection with the lymphatics.

c

The thin layer of cells that makes up the interior lining of the blood vessels is called the _____. a. mucosa b. epithelium c. endothelium d. connective tissue e. lymphoid tissue.

c

Toll-like receptors are located _____. a. only on the plasma membrane b. on the plasma membrane and the mitochondrial outer membrane c. on the plasma membrane and endosomal membranes d. only in the cytoplasm e. inside inflammasomes.

a

Unlike inflammatory cytokines, Toll-like receptors _____. a. are never secreted b. participate only in adaptive immune responses c. are expressed only by dendritic cells d. stimulate the production of acute-phase proteins e. induce fever.

b

Vaccination is best described as prevention of severe disease by _______. a. the deliberate introduction of a virulent strain of an infectious agent b. prior exposure to an infectious agent in an attenuated or weakened form c. prophylactic treatment with antibiotics d. stimulating effective innate immune responses e. using effective public-health isolation regimens such as quarantine.

Innate immune responses are initiated almost immediately after infection, whereas adaptive immunity takes longer to develop. Innate immunity uses generalized and invariant mechanisms to recognize pathogens. Examples of these are the receptors on phagocytes that recognize surface molecules shared by many different pathogens and stimulate phagocytosis, and serum proteins such as complement. Innate immunity is often unable to eradicate the pathogen completely, and even when it does, it does not produce immunity to reinfection. An adaptive immune response, in contrast, involves specific recognition of the particular pathogen by highly specific receptor on a subset of lymphocytes, which are selected from a pool of millions of lymphocytes each bearing receptors specific for different molecules. Adaptive immunity is often powerful enough to eradicate the infection and provides long-term protective immunity through immunolog

What are the main differences between innate immunity and adaptive immunity?

e

When effector lymphocytes secrete _____, an inflammatory response ensues. a. lysozyme b. defensins c. lymph d. sebum e. cytokines.

a, d

Which of the following Toll-like receptors are expressed exclusively in NK cells? (Select all that apply.) a. TLR3 b. TLR4 c. TLR7 d. TLR8 e. TLR9.

a,c,e

Which of the following are characteristics of innate immunity: a. inflammation b. improvement in recognition of the pathogen during the response c. fast response d. highly specific for a particular pathogen e. cytokine production.

d

Which of the following are important in anchoring the membrane-attack complex to the membrane? a. C3 and C5 b. C5 and C6 c. C6 and C7 d. C7 and C8 e. C8 and C9.

14 c, d

Which of the following cleaves C2? (Select all that apply.) a. Factor B b. C1r c. MASP-2 d. C1s e. C4b.

a

Which of the following complement components is an opsonin that binds to complement receptor 1 (CR1) on macrophages? a. C3b b. C3a c. Bb d. Ba e. C3bBb.

b

Which of the following does not accurately describe complement components? a. soluble proteins b. made by the spleen c. located in extracellular spaces d. some function as proteases once activated e. activated by a cascade of enzymatic reactions.

d

Which of the following does not describe a feature observed when a target cell is induced to commit apoptosis by an NK cell? a. DNA fragmentation by target cell nucleases b. target cell shrinkage c. shedding of membrane-enclosed vesicles by the target cell d. chromatin extrusion in the form of decondensed DNA by the target cell e. macrophage disposal of apoptotic remains of the target cell.

d

Which of the following does not describe a safety mechanism to ensure that only infected cells are attacked by NK cells? a. The default state is one of active inhibition, which must be overcome by activating signals before killing occurs. b. Intimate contact with target cells is required. c. No single receptor-ligand interaction induces cytotoxicity, but instead many combinations of receptor-ligand interactions influence the decision to kill or not to kill a target cell. d. All of the above are safety are safety features that have evolved to prevent NK cells from attacking healthy cells.

a

Which of the following does not describe defensins? a. highly conserved with few variants b. contain a large proportion of arginine residues c. contain three intra-chain disulfide bonds d. amphipathic, with hydrophobic and hydrophilic regions e. disrupt pathogen membranes by penetrating them and disrupting their integrity.

b

Which of the following does not describe the actions of the coagulation system? a. blood clot formation b. enhancement of dissemination of microbes into lymphatics and bloodstream c. decrease in blood loss and fluid into interstitial spaces in tissues d. release of inflammatory mediators by platelets e. wound healing.

e

Which of the following explains why immunity to influenza may appear to be relatively short-lived? a. Effective immunological memory fails to develop. b. Immune responses to influenza involve innate immune mechanisms only. c. The primary and secondary immune responses are equivalent. d. Influenza virus targets memory cells. e. New influenza variants able to escape previous immunity appear regularly.

c

Which of the following is not associated with mobilization of neutrophils to infected tissue? a. TNF-\alpha production by macrophages b. upregulation of selectins on blood vessel endothelium c. interferon response d. generation of a CXCL8 gradient e. extravasation across endothelium f. proteolysis of basement membrane of blood vessels.

d

Which of the following is not associated with mucosal surfaces? a. mucus-secreting goblet cells b. lysozyme c. M cells d. white pulp e. beating cilia.

e

Which of the following is the membrane-bound form of C3 convertase of the alternative pathway of complement activation? a. iC3 b. C3a c. C3b d. iC3Bb e. C3bBb.

d

Which of the following is the soluble form of C3 convertase of the alternative pathway of complement activation? a. iC3 b. iC3b c. C3b d. iC3Bb e. C3bBb.

a

Which of the following pairs is mismatched? a. innate immunity: highly specialized defenses b. secondary immune response: immunological memory c. hematopoiesis: bone marrow d. phagocytosis: uptake and killing of microbes e. lymphocyte recirculation: continuous transport between blood and lymph.

a

Which of the following pairs is mismatched? a. lymphocytes: innate immune response b. natural killer cell: kills virus-infected cells c. macrophage: phagocytosis and killing of microorganisms d. erythrocyte: oxygen transport e. eosinophil: defense against parasites.

e

Which of the following pairs is mismatched? a. monocyte progenitor: macrophage b. erythroid progenitor: megakaryocyte c. myeloid progenitor: neutrophil d. lymphoid progenitor: natural killer cell. e. None of the above is mismatched.

e

Which of the following pairs is mismatched? a. primary granules: azurophilic granules b. secondary granules: unsaturated lactoferrin c. azurophilic granules: myeloperoxidase d. gelatinase: iron sequestration e. tertiary granules: natural killer cells.

a

Which of the following pairs of associations is mismatched? a. large granular lymphocyte: T cell b. megakaryocyte: platelet c. B cell: plasma cell c. monocyte: macrophage d. myeloid progenitor: neutrophil.

e

Which of the following polymerizes to form a transmembrane channel that compromises the integrity of cell membranes? a. C5 b. C6 c. C7 d. C8 e. C9.

b, d

Which of the following statements are correct? a. Macrophages are granulocytes. b. Macrophages derive from monocytes. c. Macrophages are non-phagocytic. d. Macrophages reside in the tissues. e. All of the above statements are false.

b

Which of the following statements is false? a. During human development, hematopoiesis takes place at different anatomical locations. b. The hematopoietic stem cell gives rise to white blood cells, but a different stem cell is the progenitor of red blood cells. c. Hematopoietic stem cells are self-renewing. d. Platelets participate in clotting reactions to prevent blood loss. e. Megakaryocytes do not circulate and reside only in the bone marrow.

b

Which of the following statements regarding neutrophils is false? a. Neutrophils are mobilized from the bone marrow to sites of infection when needed. b. Neutrophils are active only in aerobic conditions. c. Neutrophils are phagocytic. d. Neutrophils form pus, which comprises dead neutrophils. e. Dead neutrophils are cleared from sites of infection by macrophages.

c

Which of the three complement pathways becomes activated soonest after an initial infection? a. the classical pathway b. the lectin pathway c. the alternative pathway.

Before the establishment of an effector population of lymphocytes, several events must occur: (1) specific recognition of pathogen by lymphocyte receptors (clonal selection); (2) proliferation of pathogen-specific lymphocytes to expand responding populations (clonal expansion); and (3) differentiation into effector lymphocytes with the resulting establishment of an organized adaptive immune response.

Why does it take approximately a week after infection for the benefits of an adaptive immune response to start to be felt?

15 b

With which of the following complement proteins does C-reactive protein interact? a. factor D b. C1 c. factor P d. C4 e. C2.

b

_____ act as cellular messengers by delivering degraded pathogens to lymphoid organs. a. Plasma cells b. Dendritic cells c. Large granular lymphocytes d. Mast cells e. Basophils.

c

_____ are soluble complement fragments that mediate localized and systemic inflammatory responses. a. cryptdins b. defensins c. anaphylatoxins d. selectins e. C-reactive proteins.

c

_____ cells persist long after an individual has been vaccinated. a. Neutrophil b. Plasma c. Memory d. M e. Mast.

b

_____ help to prevent systemic bacterial dissemination by producing chromatin structures loaded with antimicrobial substances. a. Inflammasomes b. Neutrophil extracellular traps c. RIG-1-like helicases d. Granulomas e. Plasmacytoid dendritic cells.

a

_____ is a cytokine produced by both macrophages and dendritic cells that promotes the proliferation, differentiation, and survival of NK cells. a. IL-15 b. IL-1\beta c. CXCL8 d. TNF-\alpha e. IL-6.

b

_____ is not an opsonin. a. Mannose-binding lectin b. IFN-\alpha c. C-reactive protein d. surfactant protein-A (SP-A) e. surfactant protein-D (SP-D).

a,e

_____ is/are needed to minimize the damaging effects to neighboring host cells during a respiratory burst. (Select all that apply.) a. Catalase activity b. Complement control proteins c. NADPH oxidase activity d. Neutrophil mobilization e. Superoxide dismutase activity.