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Immunobiology 9th Edition By by Kenneth Murphy -Test Bank

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Immunobiology 9th Edition By by Kenneth Murphy -Test Bank

Janeway’s Immunobiology, 9th Edition

Chapter 10: The Humoral Immune Response

B-cell activation by antigen and helper T cells

10-1 Activation of B cells by antigen involves signals from the BCR and either TFH cells or microbial antigens

10.1 Multiple choice: A mouse is immunized with the tetanus toxoid protein (inactivated toxin) in adjuvant. One week later, the entire population of splenic B cells are isolated from the mouse and mixed with tetanus toxoid-specific CD4 TFH cells plus the purified tetanus toxoid protein. Four days later, the total number of B cells in the culture and the number of tetanus toxoid-specific B cells are determined and compared to the starting population on the day of isolation. The results are shown in Figure Q10.1.

Figure Q10.1

The tetanus-specific B cells preferentially survive and proliferate because:

  1. They are the only B cells that express CD40.
  2. They are the only B cells that express the receptor for IL-21.
  3. They are the only B cells that proliferate in response to their antigen.
  4. They are the only B cells presenting the tetanus peptide to the TFH cells.
  5. They are the only B cells that received a TLR stimulus during priming.

10-2 Linked recognition of antigen by T cells and B cells promotes robust antibody responses

10.2 Multiple choice: The vaccine to Haemophilus influenzae type b is called a conjugate vaccine. 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:

  1. Antibodies to the bacterial polysaccharide and the tetanus toxoid
  2. Antibodies to the tetanus toxoid only
  3. Antibodies to the bacterial polysaccharide only
  4. Antibodies that only bind to the protein-polysaccharide conjugate in the vaccine
  5. Antibodies that recognize the polysaccharide capsule when shed by the bacteria

10-3 B cells that encounter their antigens migrate toward the boundaries between B-cell and T-cell areas in secondary lymphoid tissues

10.3 Short answer: When vesicular stomatitis virus (VSV) is used to infect mice via footpad injection, viral particles are trapped in the draining lymph node (the popliteal lymph node) within 5 minutes of injection. These viral particles are then retained in the lymph node for many hours, where they can be visualized on cells that are interacting with B cells. The cells retaining the viral particles in the lymph node are not tissue-resident dendritic cells that have migrated to the lymph node with the virus, as this process takes much longer than 5 minutes. In which region of the lymph node would you expect to find the trapped viral particles and on which cells?

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:

  1. No defects in any type of antibody response
  2. Defects in the initial activation of all B cells
  3. A lack of discrete B cell and T cell zones in the lymphoid organ
  4. A defect in T cell-dependent antibody responses
  5. An increased number and size of germinal centers

10-4 T cells express surface molecules and cytokines that activate B cells, which in turn promote TFH-cell development

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:

  1. A defect in antibody responses to EBV due to impaired T cell help for B cells
  2. A defect in adhesion of cytotoxic T cells to EBV-infected B cells
  3. Impaired migration of activated B cells to the germinal center
  4. Impaired survival of activated B cells, normally induced by CD40 stimulation
  5. A defect in TFH differentiation, normally induced by ICOS on B cells binding to ICOS-ligand on TFH cells

10-5 Activated B cells differentiate into antibody-secreting plasmablasts and plasma cells

10.6 True/False: Once B cells begin secreting antibodies, they cease dividing and have a life-span of only a few days.

10-6 The second phase of a primary B-cell immune response occurs when activated B cells migrate into follicles and proliferate to form germinal centers

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:

  1. When B cells cycle between the dark zone and the light zone of the germinal center
  2. When B cells leave the germinal center and migrate through the T-cell zone on their way to the blood
  3. When B cells migrate and form a primary focus of antibody-secreting plasmablasts in the medullary cords of the lymph node
  4. When B cells migrate to the border between the T-cell zone and the B-cell zone of the lymph node
  5. When B cells up-regulate CXCR4 and migrate into the dark zone of the germinal center

10-7 Germinal center B cells undergo V-region somatic hypermutation, and cells with mutations that improve affinity for antigen are selected

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:

  1. Mutations that decrease the antibody affinity lead to an arrest of B cell proliferation.
  2. B cells making higher affinity antibodies receive more help from TFH cells.
  3. Somatic hypermutations only take place in the sequences encoding the CDR1, CDR2, and CDR3 regions.
  4. Mutations that increase antibody affinity lead to an increased rate of B cell proliferation.
  5. The majority of nucleotide changes introduced by AID don’t change the amino acid coding sequence.

10-8 Positive selection of germinal center B cells involves contact with TFH cells and CD40 signaling

10.9 Multiple choice: Studies show that about 50–100 different B cells initially seed each germinal center (d7 post-infection). These different B cells are represented by different colored circles in a white oval (germinal center) in Figure Q10.9. Which of the choices shown best represents the B cell population that would be found in the same germinal center approximately two weeks later?

Figure Q10.9

10-9 Activation-induced cytidine deaminase (AID) introduces mutations into genes transcribed in B cells

10.10 Short answer: Mice and humans with inactivating mutations in the gene encoding activation-induced cytidine deaminase (AID) have an immunodeficiency disease known as ‘hyper IgM type 2’. Since AID is the enzyme that catalyzes the conversion of cytosines in the DNA to uracils, thereby initiating the process of somatic hypermutation, why do individuals with this deficiency only produce IgM antibodies?

10-10 Mismatch and base-excision repair pathways contribute to somatic hypermutation following initiation by AID

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:

  1. Following AID action, a double-stranded DNA break plus chewing back of the ends occurs before re-ligation of the sequence.
  2. The error-prone polymerase repairs the sequence by inserting random nucleotides.
  3. There are two different pathways of repair target, one targeting G:C and one targeting A:T base pairs.
  4. B cells are the only cells to express the enzyme uracil-DNA glycoslyase (UNG).
  5. During active transcription both A:T and G:C base pairs are temporarily single-stranded.

10-11 AID initiates class switching to allow the same assembled VH exon to be associated with different CH genes in the course of an immune response

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:

  1. The processed RNA from the switch region guides AID to this site in the DNA
  2. The binding of DNA-PK’s to the switch region sequence in the DNA
  3. The presence of double-stranded breaks in the DNA in this region
  4. The binding of AID to the RNA polymerase that is transcribing the switch region
  5. The predominance of G:C base pairs in the switch sequence

10-12 Cytokines made by TFH cells direct the choice of isotype for class switching in T-dependent antibody responses

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:

  1. Germinal center stromal cells
  2. Other B cells in the germinal center
  3. Follicular dendritic cells in the germinal center
  4. Any CD4 T cell in the same lymph node
  5. TFH cells in the germinal center

10-13 B cells that survive the germinal center reaction eventually differentiate into either plasma cells or memory cells

10.14 Short answer: Irradiation of mice with a dose of 600 rad of total body irradiation eliminates 95% of total lymphocytes from spleen and lymph nodes and also eliminates all antigen-specific memory B cells. Nonetheless, when Influenza A-infected mice are subjected to this irradiation at 60-days post-infection, and then reconstituted with bone marrow cells from a naive mouse (this replenishes all of the lymphocyte populations), the levels of circulating anti-Influenza A IgG antibodies show nearly no decline when mice are monitored for the following year. What is the explanation for this finding?

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:

  1. Their interactions with TFH cells specific for pathogens that infect the gut
  2. The lack of germinal centers in the mucosal lymphoid organs
  3. The absence of S1PR1 expression on IgA-secreting plasma cells
  4. Their priming and differentiation in mucosal lymphoid organs
  5. Their inability to access the bone marrow compartment

10-14 Some antigens do not require T-cell help to induce B-cell responses

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:

  1. Adults are likely exposed to more different strains (serotypes) of pneumoniae than infants.
  2. Adult B cells don’t require TFH cells to make antibody responses.
  3. Infant B cells are immature and don’t respond to TI-2 antigens.
  4. Adult B cells respond more robustly than infant B cells to B-cell mitogens.
  5. Infant B cells are more dependent on the cytokine BAFF.

The distributions and functions of immunoglobulin classes

10-15 Antibodies of different classes operate in distinct places and have distinct effector functions

10.17 Short answer: Borrelia hermsii is a spirochete bacterium, transmitted by tick bites, that causes an illness characterized by a relapsing fever. The bacteria enter the host bloodstream and replicate there. Studies in mice show that episodes of bacteremia (bacteria in the blood) are efficiently controlled by anti-bacterial antibodies, but interestingly, follicular B cells are not required for this response, nor is the response impaired by splenectomizing the mice (i.e., removing the spleen). Which B cells are most likely responsible for this antibody response?

10.18 Multiple choice: Individuals with a genetic polymorphism in the Fcg receptor, FcgRIIa (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 FcgRIIa bind to the constant region of this receptor’s target antibody. The reason this FcgRIIa-dependent response it the major form of protection against Neisseria meningitidis is because:

  1. T cells are unable to enter the brain and spinal cord.
  2. Mast cells are unable to localize to the meninges.
  3. IgG antibodies are the major isotype able to diffuse into tissues.
  4. IgM antibodies do not have high enough affinity to provide protection.
  5. Neutrophils are unable to phagocytose encapsulated bacteria.

10-16 Polymeric immunoglobulin receptor binds to the Fc regions of IgA and IgM and transports them across epithelial barriers

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:

  1. Fc receptor, FcgRIIa
  2. Complement receptor, CR1
  3. TLR adapter protein, MyD88
  4. Poly Ig receptor
  5. AID

10-17 The neonatal Fc receptor carries IgG across the placenta and prevents IgG excretion from the body

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.

  1. Newborn infants are not exposed to bacterial pathogens for the first 4–6 months of life.
  2. Newborn infants are born with high circulating levels of complement proteins to protect them.
  3. Newborn infants are born with high circulating levels of antimicrobial peptides to protect them.
  4. Newborn infants are vaccinated against these common bacterial pathogens.

10-18 High-affinity IgG and IgA antibodies can neutralize toxins and block the infectivity of viruses and bacteria

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:

  1. Having a high degree of multi-valency, such as being a pentamer or hexamer of immunoglobulin monomers
  2. Having high affinity for the antigen
  3. Being present at a high concentration in the circulation
  4. Being efficient at activating the complement cascade
  5. Having a long half-life in the body

10-19 Antibody:antigen complexes activate the classical pathway of complement by binding to C1q

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:

  1. The IgG antibodies bind to a multivalent soluble antigen in solution, such as a polysaccharide structure shed from a bacterial pathogen.
  2. The IgG antibodies bind to a viral capsid protein that is present in more than 100 copies on the viral particle surface.
  3. The IgG antibodies bind to a bacterial surface by recognizing a repetitive polysaccharide component of the bacterial capsule.
  4. The IgG antibodies are binding self-antigens such as chromatin released from dead cells.
  5. The IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin.


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