Immuno Chapter 10
10.25 Multiple choice: Some individuals with repetitive exposure to high doses of Schistosoma mansoni develop resistance to re-infection by this helminthic parasite. In contrast, other individuals remain highly susceptible. Population studies showed that resistant individuals had increased numbers of circulating eosinophils in their blood compared to susceptible individuals, and further, that these eosinophils had increased levels of: A. Complement receptor, CR1 B. Mannose binding lectin C. Fc(epsilon)RII, the low affinity IgE receptor D. Fc(gamma)RII-B, the inhibitor IgG receptor E. Anti-microbial ficolins
C. Fc(epsilon)RII, the low affinity IgE receptor
10.2 Multiple choice: The vaccine to Haemophilus influenzae type b is called a conjugatevaccine. It is composed of the tetanus toxoid protein conjugated to the capsular polysaccharide of the H. influenzae type b bacteria. When used to vaccinate infants, the antibody response generated by this vaccine would include: A. Antibodies to the bacterial polysaccharide and the tetanus toxoid B. Antibodies to the tetanus toxoid only C. Antibodies to the bacterial polysaccharide only D. Antibodies that only bind to the protein-polysaccharide conjugate in the vaccine E. Antibodies that recognize the polysaccharide capsule when shed by the bacteria
A. Antibodies to the bacterial polysaccharide and the tetanus toxoid
10.18 Multiple choice: Individuals with a genetic polymorphism in the Fc receptor, FcRIIa (CD32), have an increased susceptibility to bacterial meningitis (inflammation of the membranes (meninges) surrounding the brain and spinal cord) caused by the encapsulated bacterium, Neisseria meningitidis. This polymorphism reduces the efficiency with which the phagocytes expressing FcRIIa bind to the constant region of this receptor's target antibody. The reason this FcRIIa-dependent response it the major form of protection against Neisseria meningitidis is because: A. T cells are unable to enter the brain and spinal cord. B. Mast cells are unable to localize to the meninges. C. IgG antibodies are the major isotype able to diffuse into tissues. D. IgM antibodies do not have high enough affinity to provide protection. E. Neutrophils are unable to phagocytose encapsulated bacteria.
C. IgG antibodies are the major isotype able to diffuse into tissues.
10.16 Multiple choice: Two different vaccines have been developed that protect vaccinated individuals against pneumococcal disease, a bacterial infection that causes pneumonia, meningitis and sepsis (blood stream infection). This disease is caused by the bacteria, Streptococcus pneumoniae. One vaccine, PPSV23, is a mixture of polysaccharides isolated from 23 different serotypes of S. pneumoniae. The second vaccine, PCV13, is a conjugate vaccine made from polysaccharides of 13 different serotypes of the bacteria conjugated to diphtheria toxoid (inactivated toxin protein). The PPSV23 vaccine is only given to adults, whereas infants and small children are given PCV13. This is because: A. Adults are likely exposed to more different strains (serotypes) of S. pneumoniae than infants. B. Adult B cells don't require TFH cells to make antibody responses. C. Infant B cells are immature and don't respond to TI-2 antigens. D. Adult B cells respond more robustly than infant B cells to B-cell mitogens. E. Infant B cells are more dependent on the cytokine BAFF.
C. Infant B cells are immature and don't respond to TI-2 antigens.
10.4 Multiple choice: CXCR5 is the receptor for the chemokine CXCL13, secreted by follicular stromal cells and follicular dendritic cells in the B cell zones (i.e., lymphoid follicles) of secondary lymphoid organs. A conditional knockout mouse in which CXCR5 was specifically deleted only in T cells would have: A. No defects in any type of antibody response B. Defects in the initial activation of all B cells C. A lack of discrete B cell and T cell zones in the lymphoid organ D. A defect in T cell-dependent antibody responses E. An increased number and size of germinal centers
D. A defect in T cell-dependent antibody responses
10.19 Multiple choice: Wild-type mice infected with one strain of Influenza A virus (PR8) by intranasal inoculation are protected from intranasal infection by a related Influenza A virus (Beijing), a phenomenon known as cross-protection. These infections are generally localized to the upper respiratory tract. Mice with a homozygous single gene defect in 'gene X' have greatly impaired cross-protection to Influenza A-Beijing following immunization with Influenza A-PR8 by the intranasal route. Gene X likely encodes: A. Fc receptor, FcRIIa B. Complement receptor, CR1 C. TLR adapter protein, MyD88 D. Poly Ig receptor E. AID
D. Poly Ig receptor
10.12 Multiple choice: Unlike somatic hypermutation, class switching occurs in discrete sequence regions upstream of the immunoglobulin heavy chain coding sequences (called switch regions). One key element in directing the enzyme AID to a specific switch region is the opening of the DNA duplex combined with polymerase stalling during active transcription in that region. A second key feature of directing AID to a specific switch region is: A. The processed RNA from the switch region guides AID to this site in the DNA B. The binding of DNA-PK's to the switch region sequence in the DNA C. The presence of double-stranded breaks in the DNA in this region D. The binding of AID to the RNA polymerase that is transcribing the switch region E. The predominance of G:C base pairs in the switch sequence
A. The processed RNA from the switch region guides AID to this site in the DNA
10.7 Multiple choice: The germinal center is a region within the secondary B cell follicle where sustained B cell proliferation and differentiation take place. The processes of B cell proliferation and differentiation, including affinity maturation and class switching, require periodic interactions of the germinal center B cells with CD4 TFH cells. These periodic interactions between the B cells and TFH cells can occur: A. When B cells cycle between the dark zone and the light zone of the germinal center B. When B cells leave the germinal center and migrate through the T-cell zone on their way to the blood C. When B cells migrate and form a primary focus of antibody-secreting plasmablasts in the medullary cords of the lymph node D. When B cells migrate to the border between the T-cell zone and the B-cell zone of the lymph node E. When B cells up-regulate CXCR4 and migrate into the dark zone of the germinal center
A. When B cells cycle between the dark zone and the light zone of the germinal center
10.5 Multiple choice: Patients with the disease X-linked lymphoproliferative syndrome (XLP) lack expression of the small adapter protein SAP, which associates with receptors of the SLAM family. One characteristic of this disease is an inability of cytotoxic T cells to control infections with a virus, Epstein-Barr virus (EBV), that replicates in B cells. This defect in control of EBV results from: A. A defect in antibody responses to EBV due to impaired T cell help for B cells B. A defect in adhesion of cytotoxic T cells to EBV-infected B cells C. Impaired migration of activated B cells to the germinal center D. Impaired survival of activated B cells, normally induced by CD40 stimulation E. A defect in TFH differentiation, normally induced by ICOS on B cells binding to ICOS-ligand on TFH cells
B. A defect in adhesion of cytotoxic T cells to EBV-infected B cells
10.8 Multiple choice: In germinal centers, proliferating B cells undergo a process called somatic hypermutation, in which mutations are introduced into the V regions of the antibody heavy and light chain genes. When this process is complete after several weeks, the overall affinities of the antibodies produced are greatly increased compared to those present early in the primary response. The somatic hypermutation process leads to increased antibody affinity because: A. Mutations that decrease the antibody affinity lead to an arrest of B cell proliferation. B. B cells making higher affinity antibodies receive more help from TFH cells. C. Somatic hypermutations only take place in the sequences encoding the CDR1, CDR2, and CDR3 regions. D. Mutations that increase antibody affinity lead to an increased rate of B cell proliferation. E. The majority of nucleotide changes introduced by AID don't change the amino acid coding sequence.
B. B cells making higher affinity antibodies receive more help from TFH cells.
10.21 Multiple choice: Neutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (i.e., the tetanus toxoid). The most important feature of a neutralizing antibody is: A. Having a high degree of multi-valency, such as being a pentamer or hexamer of immunoglobulin monomers B. Having high affinity for the antigen C. Being present at a high concentration in the circulation D. Being efficient at activating the complement cascade E. Having a long half-life in the body
B. Having high affinity for the antigen
10.24 Multiple choice: The upper respiratory tract of many individuals is colonized by Streptococcus pneumoniae bacteria. Infections caused by these bacteria, including pneumonia, meningitis, otitis media (ear infections), and sinusitis, are thought to occur in individuals lacking protective antibodies. For many years, IgG was thought to be the major antibody class responsible for protective immunity to S. pneumoniae, due to the ability of anti-bacterial capsule IgG antibodies to opsonize the bacteria and promote phagocytosis. However, in addition to IgG, pneumococcal polysaccharides elicit robust IgA antibody responses. It was traditionally thought that these IgA antibodies functioned in neutralization, by blocking bacterial attachment to mucosal epithelial cells. It is now known that IgA antibodies, like IgG, can function as opsonins, to induce phagocytosis and killing of IgA-coated pathogens. This function of IgA antibodies depends on: A. The production of high affinity anti-bacterial IgA antibodies B. The dimeric form of IgA antibodies to bind to multivalent sites on the bacteria C. The ability of dimeric IgA binding to recruit and activate the complement cascade D. The presence of IgA-specific Fc receptors on neutrophils and macrophages E. The ability of IgA antibodies to efficiently cross the epithelial surface and enter the airways
D. The presence of IgA-specific Fc receptors on neutrophils and macrophages
10.15 Multiple choice: In humans, IgA is produced in copious amounts, estimated to be a rate of 3 g/day. Nearly all of the IgA secreting plasma cells are found in the gastrointestinal (GI) tract where the secreted IgA is transported across the GI epithelium into the lumen of the gut. There, this antibody protects the GI epithelium against intestinal pathogens. In contrast, none of the GI resident long-lived antibody secreting cells produce antibodies of the IgG class. The differential localization of long-lived antibody secreting cells producing IgA compared to those producing IgG is likely due to: A. Their interactions with TFH cells specific for pathogens that infect the gut B. The lack of germinal centers in the mucosal lymphoid organs C. The absence of S1PR1 expression on IgA-secreting plasma cells D. Their priming and differentiation in mucosal lymphoid organs E. Their inability to access the bone marrow compartment
D. Their priming and differentiation in mucosal lymphoid organs
10.13 Multiple choice: In cell culture experiments, purified B cells expressing IgM can be induced to switch to producing IgE by stimulating them with an antibody to CD40 (a stimulatory antibody) plus the cytokine IL-4. In an individual undergoing an immune response, these signals would normally be provided by: A. Germinal center stromal cells B. Other B cells in the germinal center C. Follicular dendritic cells in the germinal center D. Any CD4 T cell in the same lymph node E. TFH cells in the germinal center
E. TFH cells in the germinal center
10.22 Multiple choice: IgM antibodies are much more efficient than IgG at activating the complement cascade. However, under certain circumstances, IgG antibodies will activate the complement pathway. One example of a situation in which IgG binding to its antigen will not trigger the complement cascade is when: A. The IgG antibodies bind to a multivalent soluble antigen in solution, such as a polysaccharide structure shed from a bacterial pathogen. B. The IgG antibodies bind to a viral capsid protein that is present in more than 100 copies on the viral particle surface. C. The IgG antibodies bind to a bacterial surface by recognizing a repetitive polysaccharide component of the bacterial capsule. D. The IgG antibodies are binding self-antigens such as chromatin released from dead cells. E. The IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin.
E. The IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin.
10.6 True/False: Once B cells begin secreting antibodies, they cease dividing and have a life-span of only a few days.
False
10.26 Multiple choice: Antibody-dependent cell-mediated cytotoxicity (ADCC) is an important effector mechanism in immunity to virus infections. This immune pathway has also been exploited for clinical applications. For instance, patients with various disorders, including rheumatoid arthritis and some B cell lymphomas, are treated with an antibody directed at CD20, a surface receptor expressed on all B cells. This antibody leads to the depletion of B cells from the patients by the actions of: A. Natural killer (NK) cells B. Cytotoxic CD8 T cells C. Cytotoxic CD4 T cells D. Activated macrophages E. The complement cascade membrane attack complex
A. Natural killer (NK) cells
10.20 Multiple choice: Infants born with the immunodeficiency disease X-linked agammaglobulinemia (XLA) have a block in B cell development, and fail to produce mature B cells. As a result, these infants lack the ability to produce antibodies. After birth, babies with XLA first begin to show symptoms of recurrent and persistent extracellular bacterial infections due to common environmental pathogens when they are 4-6 months of age. The reason these infants are healthy for the first 4-6 months after birth is because:Newborn infants have high circulating levels of maternal IgG at birth. A. Newborn infants are not exposed to bacterial pathogens for the first 4-6 months of life. B. Newborn infants are born with high circulating levels of complement proteins to protect them. C. Newborn infants are born with high circulating levels of antimicrobial peptides to protect them. D. Newborn infants are vaccinated against these common bacterial pathogens
A. Newborn infants are not exposed to bacterial pathogens for the first 4-6 months of life.
10.11 Multiple choice: The process of somatic hypermutation of antibody V regions sequences is initiated by the enzyme AID. This enzyme targets cytidine residues in the DNA sequence that are normally part of a G:C pair in the double-stranded DNA. Yet the hypermutation process generates mutations at both G:C and A:T base pairs of the original sequence because: A. Following AID action, a double-stranded DNA break plus chewing back of the ends occurs before re-ligation of the sequence. B. The error-prone polymerase repairs the sequence by inserting random nucleotides. C. There are two different pathways of repair target, one targeting G:C and one targeting A:T base pairs. D. B cells are the only cells to express the enzyme uracil-DNA glycoslyase (UNG). E. During active transcription both A:T and G:C base pairs are temporarily singlestranded.
C. There are two different pathways of repair target, one targeting G:C and one targeting A:T base pairs.
10.28 Multiple choice: The W/Wv mouse strain is heterozygous for two different alleles of the gene encoding the growth factor receptor, c-kit, an important receptor expressed on hematopoietic progenitor cells in the bone marrow. The major defect in these mice is the absence of single lineage of hematopoietic cells. When these mice are challenged with larval Haemaphysalis longicornis ticks, they fail to become resistant to the ticks, in spite of generating high titers of anti-tick IgE antibodies. The cell type missing in the W/Wv mice is most likely:Natural Killer (NK) cells A. Eosinophils B. Tissue-resident dendritic cells C. Tissue-resident macrophages D. Tissue-resident mast cells
D. Tissue-resident mast cells
