if any body wants answres plz kieep message here chose the best single answer part-1 1. Central (primary) lymphoid organs a. are efficient in exposing T cells to foreign antigen. b. are the primary site of antibody synthesis and release. c. filter blood and trap blood-borne antigens. d. provide the microenvironment for maturation of T and B cells. e. line the mucosal surfaces of the body for efficient antigen contact. 2. Hematopoietic stem cells are pluripotent, which means that they are a. antigen-specific cells. b. capable of developing into any blood cells. c. committed to produce cells of a single lineage. d. not self-renewing. e. T and B lymphocytes of many different antigen specificities. 3. Lymphocytes continually recirculate through peripheral lymphoid tissue in order to a. be killed before they cause autoimmunity. b. efficiently encounter antigen. c. mature from stem cells into lymphocytes. d. phagocytose antigen and kill it. e. go where no cell has gone before. 4. Peripheral lymphoid organs a. are centrally located in the abdomen to protect their vital functions. b. are designed to maximize contact between antigen and lymphocytes. c. produce antigen-specific lymphocytes from stem cells in response to antigen. d. sequester antigen to minimize its damage to the body. e. store large numbers of activated effector cells for a rapid response to antigen. 5. The PRIMARY purpose of the adaptive immune system is to a. block all pathogens from entering the body. b. cure allergic reactions. c. kill tumor cells. d. protect from disease upon re-infection with a specific pathogen. e. reject foreign transplants. 6. Rapid but non-antigen specific immune responses are produced by the a. adaptive immune system. b. innate immune system. c. leukocytes. d. lymphatic system. e. memory response. 7. Vaccination protects us from infectious disease by generating memory a. antigen. b. lymphocytes. c. macrophages. d. PMNs. e. stem cells. 8. Which situation below describes an example of innate immunity? a. antibody production by plasma cells. b. antigen removal by cilia in the respiratory tract. c. complement activation by antibody bound to the surface of a bacterium. d. memory response to influenza virus e. recognition and killing of virus-infected cells by cytotoxic T cells. 9. The antigen specificity of an adaptive immune response is due to a. activation of antigen-specific lymphocytes. b. folding of antibody to fit the pathogen. c. lysis of only certain pathogens by neutrophils. d. phagocytosis of only certain pathogens by macrophages. e. production of cytokines by antigen-specific macrophages 10. Clonal selection a. begins with inflammation. b. occurs for all leukocytes. c. occurs in response to self antigens. d. results in innate immunity. e. results in proliferation of antigen-specific lymphocytes. 11. Cytokines are NOT a. able to induce increased blood vessel permeability. b. antigen-specific. c. made in response to bacterial antigens. d. signals from one cell that affects the behavior of another cell. e. secreted by macrophages. 12. A fundamental difference between the antigen receptors on B cells (BCR) and on T cells (TCR) is their a. different requirements for antigen presentation. b. function following antigen binding. c. heterogeneity from one lymphocyte to the next. d. heterogeneity on each lymphocyte. e. membrane location. 13. Genes for immunoglobulins (antibodies) are unlike other human genes in that a. antibody genes are composed of introns and exons. b. DNA for antibody molecules is inherited from only one parent. c. gene segments must be spliced together to make each unique antibody molecule. d. several exons encode each antibody molecule. e. none of the above is true. 14. Humoral immunity can be acquired passively by a. catching a virus from a friend by shaking hands. b. receiving a vaccine of influenza virus grown in eggs. c. receiving serum from someone who has recovered from an infection. d. receiving leukocytes from an immune family member. e. sharing a soda with someone who has a cold. 15. Inflammation does NOT involve a. cytokine production by macrophages. b. migration of leukocytes out of the circulation. c. pain. d. secretion of antibodies. e. swelling at the site of infection. 16. Innate immune responses are most effective against a. antigens resembling self antigens. b. common antigens on bacteria. c. genetically engineered antigens. d. viruses. e. viruses that have previously caused infection. 17. Lymphocytes acquire their antigen specificity a. as they enter the tissues from the circulation. b. before they encounter antigen. c. depending on which antigens are present. d. from contact with self antigen. e. in the secondary lymphoid organs. 18. A secondary immune response is NOT a. faster than a primary response. b. larger than a primary response. c. longer lasting than a primary response. d. more likely to result in increased adaptive immunity than a primary response. e. preceded by a longer lag period than a primary response. 19. Antibody effector functions include all of the following EXCEPT a. activating complement on bacterial surfaces to promote phagocytosis by neutrophils. b. binding extracellular viruses to block their entry into host cells. c. binding intracellular viruses to initiate cytotoxicity. d. blocking uptake of bacterial toxins by host cells. e. coating bacteria to promote their phagocytosis by neutrophils. 20. Effector functions of complement include all of the following EXCEPT a. attracting phagocytes to the site of infection. b. facilitating phagocytosis of complement-coated bacteria. c. increasing blood vessel permeability to plasma proteins. d. lysing bacterial cells. e. presenting antigen to B cells. 21. Jenner observed that milkmaids who were infected with cowpox were later immune to smallpox infections. This is an example of a(n) a. acquired immunity of barrier skin cells. b. active immunization with a non-related organism that causes similar symptoms. c. innate immunity of milkmaids to smallpox. d. memory response to a cross-reactive antigen. e. passive immunization from contact with cow's milk antibodies. 22. Macrophages generally kill the bacteria they phagocytose by fusing lysosomes containing digestive enzymes with the phagocytic vesicle. In the case of pathogens which block this fusion, pathogen killing can still be achieved through the effector function of a. B cells. b. complement. c. cytotoxic T cells. d. opsonizing antibody. e. Th1 cells. 23. Phagocytosis a. can be stimulated by antigen binding to complement or antibody. b. is an antigen-specific process. c. must be preceded by antigen processing. d. rids the body of virus-infected cells. e. only occurs after plasma cells begin secreting antibody. 24. Several friends who went on a picnic together developed vomiting and diarrhea from eating potato salad contaminated with Staphylococcus aureus enterotoxin. Effects of the toxin could best be counteracted by a. antibody binding and neutralization of the toxin. b. antibody opsonization and phagocytosis of S. aureus. c. antibody opsonization and phagocytosis of the toxin. d. B cell binding to S. aureus. e. cytotoxic T cell binding and lysis of S. aureus. 25. Which of the following statements is FALSE? a. An example of passive humoral immunity is treatment with horse anti-snake venin. b. Antigen recognized by helper T cells must be associated with Class II MHC molecules on the surface of professional APC . c. Each lymphocyte has many antigen binding receptors, each receptor capable of binding the same antigen. d. Recognition and killing of virus-infected cells by cytotoxic T cells is an example of adaptive immunity. e. The innate immune system does not deal with endogenous antigen. part-2 1. The ability of an antigen to induce an immune response does NOT depend on the antigen's a. ability to enter the thyroid. b. degree of aggregation. c. dose. d. size. e. usual presence in the body. 2. Alum is an effective adjuvant because it a. disaggregates the antigen. b. is immunogenic for stem cells c. is immunogenic for T cells. d. slows the release of antigen. e. transports antigen into the cytoplasm of antigen-presenting cells. 3. Antibody cross-reactivity is demonstrated by antibody binding to a. a cell surface marker. b. a hapten. c. a hapten-carrier complex. d. an antigen that is structurally similar to the immunogen e. the immunogen. 4. The antibiotic penicillin is a small molecule that does not induce antibody formation. However, penicillin binds to serum proteins and forms a complex that in some people induces antibody formation resulting in an allergic reaction. Penicillin is therefore a. an antigen. b. a hapten. c. an immunogen. d. both an antigen and a hapten. e. both an antigen and an immunogen. 5. Antigen entering the body in a subcutaneous injection activates its specific lymphocytes in the a. blood circulation. b. draining lymph nodes. c. MALT. d. skin. e. spleen. 6. To detect a humoral immune response to influenza virus, you would measure a. cytotoxicity of virus-infected cells in the lung. b. cytotoxicity of virus-infected cells in tissue culture. c. dividing T cells in the draining lymph nodes. d. plasma cytokine levels. e. serum antibody titer. 7. During the lag period between antigen contact and detection of adaptive immunity, a. antigen is hidden from the immune system in macrophages. b. cellular immunity can be detected but antibodies cannot. c. innate immune effectors are eliminating antigen. d. innate immunity blocks the activation of adaptive immune effector cells. e. new B and T cells with the appropriate antigen specificity must be produced in the bone marrow. 8. To elicit the best antibodies to mouse MHC I, you should inject it into a. a goat. b. a mouse of the same genetic background (strain). c. a mouse of a different strain. d. a rat. e. the mouse you isolated it from. 9. For specific antigen recognition by T cells, a. antigen is bound by a T cell membrane antibody. b. denaturation of antigen does not reduce epitope recognition. c. MHC molecules are not required. d. soluble antigen is bound directly without processing. e. antigen exposure during T cell maturation is required. 10. The immune response to a booster vaccine is called a(n) a. cellular response. b. humoral response. c. innate response. d. primary response. e. secondary response. 11. Immunogenicity a. depends on the ability of the native antigen to be presented by MHC. b. is usually a property of "self" antigens such as eye tissue. c. is not a property of antibodies. d. is not a property of haptens. e. only applies to antigens that are composed of proteins. 12. Lymphocytes are activated by antigen in the a. blood stream. b. bone marrow. c. liver. d. lymph nodes. e. skin. 13. A molecule that can be covalently linked to a non-immunogenic antigen to make it an immunogen is called a(n) a. adjuvant. b. carrier. c. hapten. d. mitogen. e. superantigen. 14. A polyclonal antibody response a. is not antigen-specific. b. is produced only in response to polymeric antigens. c. is produced by several B cells recognizing different epitopes on the same antigen. d. occurs during the lag phase of the immune response. e. violates clonal selection. 15. Very low doses of antigen may induce a. a secondary response. b. hypersensitivity. c. immunological ignorance. d. low zone tolerance. e. low zone immunity. 16. A virus vaccine that can activate cytotoxic T cells MUST contain a. a high dose of virus particles. b. an adjuvant to stimulate T cell division. c. foreign MHC. d. live virus. e. virus peptides. 17. Which statement about antigen epitopes is FALSE? a. An epitope may be shared by two different antigens. b. A protein molecule usually contains multiple epitopes. c. B cells bind only processed antigen epitopes. d. Epitopes may be linear or assembled. e. Some epitopes are more immunogenic than others 18. CD antigens a. allow leukocytes to recognize antigen. b. are each expressed on only one cell type. c. are expressed on immune cells by immunologists to "mark" them for separation. d. are found only on leukocytes. e. function as receptors for cytokine and CAMs. 19. A patient desperately needs a bone marrow transplant, and a perfect match cannot be found. The rejection response in unmatched marrow is primarily due to the presence of mature T cells that recognize the recipient's cells as foreign. To minimize this rejection response, the marrow can be treated before transfusion into the recipient with complement plus antibody to human a. CD3. b. CD4. c. CD8. d. CD28. e. CD154. 20. Antibody to membrane receptors sometimes inhibits receptor function and sometimes mimics the action of the normal receptor ligand. (For example, some antibodies to insulin receptor block the action of insulin and some mimic the action of insulin.) An antibody which should NOT either block or stimulate B cell function would be anti- a. CD21. b. CD56. c. CD80. d. Iga. e. m chain. part-3 1. Cytokines may exhibit __________ action, signaling the cells that produce them. a. antagonistic b. autocrine c. endocrine d. paracrine. e. synergistic 2. Cytokines are NOT a. antigen specific. b. capable of activating more than one cell type. c. made by lymphocytes. d. small protein molecules. e. synthesized de novo in response to antigen or other cytokines. 3. Several cytokines may have the same effect on the cells they bind. This is an example of a. a cascade. b. antagonism. c. pleiotropism. d. redundancy. e. synergy. 4. Characterization of cytokine activities is NOT made more difficult by their a. gene structure. b. pleiotropism. c. redundancy. d. secretion close to target cell membranes. e. short half-lives. 5. Interferons a. activate B cells to make virus-specific antibodies. b. are Th2 cytokines. c. are virus proteins that interfere with activation of cytotoxic T cells. d. block virus infection of host cells. e. inhibit virus replication by infected cells. 6. A cytokine can do all of the following EXCEPT a. bind to receptors which do not share cytokine-binding subunits. b. bind to its specific receptor on the same cell that produced it. c. bind to receptor antagonists produced by pathogenic viruses. d. compete with other cytokines whose receptors share signal-transducing subunits e. upregulate (increase) synthesis of high affinity subunits for its receptor. 7. Members of a cytokine receptor family a. all bind the same cytokines. b. are grouped together because they share antigen specificity c. are often found on the same cells d. are similar in protein structure and sometimes in regions of amino acid sequence. e. are specific for cytokines produced by a single cell type 8. The ability of a cytokine to change gene expression in the target cell is influenced by all of the following EXCEPT a. presence of high-affinity receptors on the target cell. b. presence of soluble cytokine receptors. c. proximity of the producing and target cells. d. rate of transport of cytokine-receptor complexes into the cytoplasm. e. simultaneous production of another cytokine whose receptor uses the same signal transducing subunit. 9. Cytokines are NOT a. able to inhibit the function of other cytokines. b. able to stimulate the synthesis of other cytokines. c. produced by more than one cell type. d. small protein molecules. e. stored in the cell for quick release. 10. The IL-2R subfamily consists of receptors for IL-2, IL-4, IL-7, IL-9, and IL-15. This group of cytokine receptors a. bind all five cytokines to promote synergistic action on target cells. b. bind cytokines which are produced by the same cell. c. each has a unique high affinity cytokine-specific a chain. d. shift the immune response towards cellular immunity. e. each has a unique signal-transducing g chain. 11. An antagonist for cytokine X may NOT be a. cytokine A competing for a shared receptor subunit. b. cytokine B which acts synergistically with cytokine X. c. cytokine C which inhibits the activation of the cell that produces cytokine X. d. made by microorganisms. e. soluble cytokine X receptors. 12. A knock-out mouse for a particular cytokine allows immunologists to characterize cytokine function a. by doing a dose-response study with competing cytokines. b. in the absence of all other cytokines. c. on all cell types simultaneously. d. under controlled conditions of local cytokine concentrations. e. with defined cell populations. 13. Activated Tc can regulate immune responses by signaling activated lymphocytes to undergo a. apoptosis. b. clonal deletion. c. clonal proliferation. d. cytotoxicity. e. somatic hypermutation. part-4 1. Complement a. is a group of active proteolytic enzymes found in serum. b. is secreted by macrophages and hepatocytes in response to antigen binding. c. participates in both innate and adaptive immune responses. d. prevents lysis of virus-infected cells. e. All of the above statements about complement are true. 2. Complement is involved in all of the following except a. attraction of neutrophils to an infection site. b. increased presence of serum proteins in the infected tissues. c. lysis of bacteria in the absence of specific antibodies. d. opsonization of microorganisms for phagocytosis. e. sensitization of T cells to antigen 3. Complement is a. activated by binding to specific complement receptors. b. antigen-specific. c. a potent promoter of virus entry into host cells. d. a series of intracellular proteins which work with antibody to eliminate endogenous antigen. e. present in the circulation in an inactive form. 4. The alternative pathway of complement activation a. causes tissue damage in the absence of C1INH. b. occurs after the classic pathway is activated. c. occurs only if the classical pathway is ineffective in pathogen clearance. d. requires C3. e. requires C4. 5. If a person is born without C2 and C4, a. C5 can still be cleaved by the classical pathway. b. C3b will not be able to bind to bacteria. c. C9 will polymerize inappropriately and lyse host cells. d. the classical pathway will be changed into the alternative pathway. e. the amount of C3b produced during bacterial infections will be reduced. 6. Which of the following are least sensitive to complement-mediated lysis? a. Enveloped viruses b. Erythrocytes c. Gram negative bacteria d. Gram positive bacteria e. Leukocytes 7. In the membrane attack phase of the classical complement pathway, the role of C5b is to a. activate the C5 convertase activity. b. attract neutrophils to lyse the pathogen. c. initiate formation of the MAC. d. polymerize into a membrane-spanning channel. e. All of these are activities of C5b. 8. Complement receptors (CR) a. activate complement on the surface of pathogens. b. bind only activated complement proteins. c. inhibit complement activation on the surface of host cells. d. on erythrocytes remove immune complexes from the circulation. e. on macrophages signal host cells to make opsonins. 9. As complement is activated by complexes of antibody-coated bacteria, bystander lysis of nearby host cells is prevented by a. a long-lived thioester bond on active complement proteins. b. covalent attachment of all active complement proteins to the pathogen surface. c. plasma proteins that inactivate the anaphylatoxins. d. proteins on host cell membranes that inhibit MAC formation. e. the slow catalytic rates of complement proteases. 10. Complement activity is restricted by all of the following EXCEPT a. dissociation of C3 and C5 convertases. b. Gram positive cell walls that are resistant to MAC polymerization. c. host cell plasma proteins that inactivate C3a, C4a, and C5a activity. d. LPS in the outer membrane of Gram negative bacteria that inactivates C3b. e. proteolytic cleavage of complement proteins into smaller fragments. 11. A deficiency in complement proteins or in their regulators can result in a. blood in the urine from erythrocyte lysis. b. decreased levels of certain complement proteins in the circulation. c. immune complex disease. d. increased numbers of infections. e. All of the above can result from complement deficiencies. part-5 1. Phagocytosis must be preceded by a. antigen binding to the phagocyte. b. chemotaxis. c. extravasation. d. integrin binding to Ig superfamily CAMs. e. oxidative burst. 2. Phagocytes bind antigen using receptors for a. C5a. b. chemokines. c. glucose. d. LPS. e. selectins. 3. Pathogens engulfed by macrophages a. are completely degraded by hydrolytic enzymes into their component amino acids and sugars. b. are degraded to small peptides and carbohydrates which are presented on Class I MHC to Tc. c. may survive and replicate in the macrophage phagocytic vesicles. d. stimulate macrophages to adhere to B cells. e. stimulate vascular endothelium to upregulate selectin expression.. 4. An inflammatory response a. is characterized by a decrease in vascular permeability. b. is stimulated by cytokines produced by neutrophils. c. occurs only during a secondary response. d. recruits phagocytes to the infection site. e. usually lasts for many weeks to ensure antigen is completely removed 5. Natural Killer cells a. are stimulated to kill infected host cells via carbohydrate-binding receptors. b. kill normal host cells with high levels of membrane MHC Class I. c. kill virus-infected cells when the virus is acquired naturally but not by immunization. d . recognize virus-infected cells by the presence of viral peptide on MHC Class II. e. secrete the complement MAC to lyse virus-infected cells. 6. Interferons a and b do NOT a. activate NK cells to kill virus-infected cells. b. get synthesized by virus-infected cells in response to infection. c. induce macrophages to increase expression of Class II MHC. d. inhibit virus replication in infected cells. e. stimulate expression of molecules required for Class I MHC presentation of viral proteins. 7. Immune system cell adhesion molecules do NOT a. allow macrophages to leave the circulation. b. allow T cells to home specifically to peripheral or mucosal lymphoid tissue. c. attract leukocytes to an infection site. d. help cytotoxic T cells to bind to their targets. e. signal neutrophils that they have arrived at an infection site. 8. Early induced immune responses are like adaptive immunity in that they a. are antigen-specific b. demonstrate immune memory. c. involve macrophages and complement. d. involve T and B lymphocytes e. use pre-synthesized proteins which can be released quickly upon cell activation. 9. Selectins a. are present on both leukocytes and vascular endothelial cells. b. bind Ig-like vascular addressins. c. include ICAM, VCAM, and MAdCAM. d. select antigen-specific lymphocytes to extravasate into the infection site. e. select antigen-specific macrophages to extravasate into the infection site. 10. Lymphocyte recirculation a. activates inflammatory cytokines to promote antigen presentation to T cells. b. allows B cells to go to the site of infection to produce antibody. c. circulates lymphokines efficiently throughout the body. d. occurs for both naïve and effector lymphocytes e. only occurs during an infection. 11. Phagocytes kill bacteria using all of the following EXCEPT a. H2O2. b. hydrolytic enzymes. c. low pH d. lysozyme. e. strong reducing agents. 12. For a circulating neutrophil to reach the site of inflammation, it must bind to blood vessel endothelial cell and then pass between the endothelial cells in a process called a. addressinazition. b. chemotaxis. c. extravasation. d. marginalization. e. opsonization. 13. Macrophages are attracted to the site of infection by all of the following EXCEPT a. bacterial peptides. b. chemokines. c. C5a. d. IL-8. e. MAdCAM. 14. Inflammatory cytokines produced by macrophages activate all of the following EXCEPT a. B cells to secrete acute phase proteins. b. integrin on leukocytes to bind more strongly to vascular CAMs. c. neutrophils to be more cytotoxic. d. NK cells to kill virus-infected cells. e. vascular endothelium to increase expression of CAMs. part-6 1. An antibody Fab contains a. complementarity determining regions. b. H and L chain variable regions. c. one antigen binding region. d. one H-L interchain disulfide bond. e. all of the above. 2. Myeloma proteins are a. abnormally formed antibodies secreted from cancerous plasma cells. b. cancerous plasma cells that divide without requiring antigen activation. c. cell lines that secrete specific antibodies for a short time, then die. d. homogeneous antibody molecules secreted by plasma cell tumors. e. protein signaling molecules that make a plasma cell become a multiple myeloma. 3. The regions of the antibody molecule which contribute MOST to the affinity of the antibody for antigen are the a. CDR. b. Fab regions. c. Fc regions. d. framework regions. e. hinge regions. 4. Antibody Fc fragments contain a. antigen-binding sites. b. CDR. c. complement-binding sites. d. framework residues. e. light chain variable domains. 5. The immunoglobulin isotype is determined by the a. antigen specificity. b. H chain constant region. c. L chain variable region. d. number of antigen-binding sites. e. number of VH domains. 6. Which statement about antigen epitopes is FALSE? a. An epitope may be shared by two different antigens. b. A protein molecule usually contains multiple epitopes. c. B cells bind only processed antigen epitopes. d. Epitopes may be linear (composed of sequential amino acids) or assembled by protein folding from amino acids far apart in the protein primary amino acid sequence. e. Some epitopes are more immunogenic than others. 7. An example of an antigen epitope from an infectious organism would be a. a bacterial endotoxin (LPS) molecule. b. a fungal cell wall protein. c. a peptide on the surface of a virus capsid protein. d. a whole virus. e. All of the above are antigen epitopes. 8. Antibody affinity for antigen depends on a. the antibody isotype. b. the complementary shape and charge of each antibody V region for its antigen epitope. c. the number of Fab regions in each antibody molecule. d. whether the antibody is in the serum or on the cell surface. e. whether the light chains are kappa or lambda. 9. Avidity a. is a pathogenic agent, causing a very serious disease. b. occurs when the ratio of antibody to antigen is optimal. c. refers to the strength of interactions between a multivalent antibody and a multivalent antigen. d. results in a loss of antibody reactivity. e. results in cross-reactivity when antibody binds two different antigens. 10. A colleague sends you an antibody to polio virus capsid protein. You perform equilibrium dialysis on the antibody to measure its affinity. Plotting r/c versus r gives you a curved line with K= 2.5 X 108 L/mole and an r intercept of 4. From these results, you conclude that the antibody is probably a. a cross-reactive antibody. b. a monoclonal anti-polio virus antibody. c. a polyclonal IgG antibody. d. IgA anti-polio virus. e. not specific for polio virus. 11. Allotypic determinants are a. constant region determinants that distinguish each Ig class and subclass within a species. b. expressed only from the paternal chromosome. c. generated by the conformation of antigen-specific VH and VL sequences. d. Not immunogenic in individuals who do not have that allotype. e. amino acid differences encoded by different alleles for the same H or L chain locus. 12. Which of the following is NOT a characteristic of IgG? a. It contains 2 g and 2 L chains b. It crosses the placenta. c. It is the predominant immunoglobulin in blood, lymph, and peritoneal fluid. d. It is the largest of all the Igs. e. Its L chains are either k or l. 13. Human serum IgA is isolated and injected into a rabbit. The rabbit anti-IgA antibodies will react against all of the following EXCEPT human a. a chain. b. IgG. c. k chain. d. l chain. e. secretory component. 14. You have purified some Fab from an IgG myeloma protein. Under appropriate conditions, you could use this Fab to generate antibodies to a. both k and l chain. b. g chain hinge region. c. J chain. d. g chain allotypic determinants. e. the idiotype of this myeloma. 15. The Ig isotype which would be most important for neutralizing polio virus before it could infect intestinal cells would be a. secretory IgA. b. serum IgA. c. serum IgD. d. serum IgG. e. membrane IgM. 16. Which of the following changes to a serum IgM antibody molecule would definitely DECREASE its avidity? a. Increase noncovalent antigen-antibody interactions in the CDR. b. Remove the secretory component. c. Replace the Fc portion of the mu chains with the Fc portion of alpha chains. d. Replace VH and VL framework regions with those from a different antibody. e. Use limited enzyme digestion to make Fab fragments. 17. IgA can be secreted from the body because it a. binds poly-Ig receptor on mucosal epithelial cells. b. has a specialized H chain called secretory chain. c. has a special secretory idiotype. d. is small enough to pass between mucosal epithelial cells and leave the body. e. is synthesized by mucosal epithelial cells and secreted directly into the intestinal lumen. 18. The ability to make antibody with the same antigen specificity but different Fc regions a. causes allelic exclusion of Ig molecules. b. does not occur against bacterial antigens. c. improves the antigen binding specificity of an Ig molecule. d. increases the effector functions of Ig molecules. e. requires clonal elimination. 19. Allergy symptoms are produced when antigen binds to IgE on FcR on a. A cells. b. macrophages. c. mast cells. d. neutrophils. e. Th1 cells. 20. One amino acid difference in the Fc region of different human g chains is the epitope recognized by anti- a. allotype. b. idiotype. c. isotype. d. IgG. e. g chain. part-7 1. Genes for immunoglobulins are unlike other human genes in that a. each polypeptide chain is encoded by several exons. b. Ig genes are composed of introns and exons c. somatic recombination occurs before mRNA is transcribed d. there is less Ig genetic material in mature B cells than in other somatic cells e. both c and d are true. 2. The gene segments needed to encode the variable region of a k chain are a. one Jk plus one Dk. b. one Jk plus one Ck. c. one Vk plus one Dk. d. one Vk plus one Jk. e. one Vk plus one Jk plus one Dk. 3. Pseudogenes are DNA sequences which look very similar to functional genes except for the presence of a(n) a. intron. b. leader sequence. c. promoter codon. d. signal sequence. e. stop codon. 4. Combinatorial diversity says that by random combination of 40 functional Vk segments with five Jk segments, the number of possible different k chains that could be made are a. 40. b. 45. c. 70. d. 200. e. 1200. 5. Which does NOT contribute to Ig antigen-binding diversity a. Any L chain can combine with any H chain to form a functional antibody. b. Any Vk can be joined to any Jk to encode the light chain V region. c. Many CH genes are present in the germline DNA. d. Random numbers of N nucleotides can be added during somatic recombination. e. VJL and VDJH joining is imprecise. 6. The proper joining of one VL to one JL is regulated by a. heptamer and nonamer sequences. b. leader sequences. c. P-nucleotide addition sites. d. 12 and 23 nucleotide spacers between heptamer and nonamer sequences. e. TdT binding site for DNA. 7. Since each B cell productively rearranges a single H and L chain allele, it exhibits a. affinity. b. allelic exclusion c. antibody restriction. d. antigen-binding diversity. e. cross-reactivity 8. Primary mRNA for H chain encodes a. one VH, one DH, and one JH segment. b. one VH, one DH, and multiple JH segments. c. multiple VH, one DH, and one JH segments. d. multiple VH, one DH, and multiple JH segments. e. multiple VH, DH, and JH segments. 9. Somatic recombination occurs a. in the bone marrow stem cell. b. in the progenitor cell as it is becoming a B cell. c. in the mature B cell following antigen contact. d. in the plasma cell after antigen contact. e. in the plasma cell after antibody secretion. 10. Junctional diversity affects primarily the amino acid sequence in a. all CDR equally. b. CDR1. c. CDR2. d. CDR3. e. FR3. 11. Isotype switching a. changes the leader sequence exon so the antibody is secreted. b. improves the antigen binding specificity of an Ig molecule. c. increases the affinity of antibodies in a process called affinity maturation. d. increases the functional diversity of Ig molecules. e. occurs randomly between switch regions. 12. Isotype switching resembles somatic recombination because both processes a. are catalyzed by the products of RAG1 and RAG2 b. are regulated by helper T cell cytokines. c. can result in stop codons in coding sequences. d. occur in developing B cells in the bone marrow. e. result in the irreversible loss of DNA from the B cell. 13. Alternative mRNA splicing a. allows the B cell to improve its antigen-binding fit after antigen contact. b. allows the B cell to make membrane IgM from the mature mRNA for secreted IgD. c. can be used for the simultaneous production of any two Ig isotypes. d. is a process by which a B cell can simultaneously synthesize m and d chains. e. occurs in response to T cell cytokines. 14. Because of the order of the CH gene segments (Cm, Cd, Cg3, Cg1, pseudogene Ce, Ca1, Cg2, Cg4, Ce, and Ca2), a human B cell which undergoes isotype switching from IgM to IgG1 can never in the future secrete a. IgA. b. IgE. c. IgG2. d. IgG3. e. IgG4. 15. Isotype switching is always productive because a. B cells produce all isotypes simultaneously. b. isotype switching does not involve recombination of DNA gene segments. c. no DNA is deleted from the chromosome in isotype switching. d. no effector diversity results from isotype switching. e. recombination between switch sites occurs in introns so it cannot introduce stop codons into coding regions. 16. Somatic hypermutation does NOT a. occur by somatic recombination. b. occur during B cell proliferation. c. occur in the B cell following antigen stimulation. d. result in increased affinity of antibodies secreted later in immune responses. e. result in the death of some B cells which no longer bind antigen. part-8 1. Which of the following is NOT True about TCR? a. All TCRs on a particular T cell have identical idiotypes. b. CDR3 of TCR has the most sequence variability from molecule to molecule. c. TCR has binding sites for both antigen and self MHC. d. TCR is a disulfide-bonded heterodimer. e. The ab or gd isotype of TCR determines the biological function of its secreted form. 2. The antigen-binding region of TCR is formed by the folding of a. Va and Vb chains. b. Va, Vb, and CD3 chains. c. Va and Vb2-microglobulin chains. d. Vg and Va chains. e. VL and VH chains. 3. Which of the following properties are NOT shared by TCR and BCR? a. Antigen-binding avidity is increased by the presence of two antigen binding regions on each receptor. b. Antigen-binding diversity is generated through gene rearrangement. c. Folding of protein domains is maintained by intrachain disulfide bonds. d. Membrane expression and lymphocyte activation by antigen require receptors to be associated with signal transduction molecules. e. Receptor antigen-binding sites are formed from two polypeptide chains. 4. TCR most closely resembles a. Class I MHC. b. Class II MHC. c. Fab region of immunoglobulin. d. Fc region of immunoglobulin. e. light chain of immunoglobulin. 5. Rearrangement of both TCR and BCR gene segments does NOT a. generate diversity of antigen binding by recombination of a large pool of germline V, D, and J segments. b. lead to CDR3 being the most hypervariable region in the receptor chains. c. require RAG-1, RAG-2, and TdT expression. d. result in allelic exclusion of membrane receptors. e. result in isotype switching after antigen stimulation of the mature lymphocytes. 6. The amount of diversity in TCR generated within one individual by somatic recombination a. is higher than BCR diversity. b. is about the same as for BCR diversity. c. is lower than BCR diversity. d. is lower than Class I MHC diversity. e. is lower than Class II MHC diversity. 7. T cells use all of the following for generating antigen-recognition diversity on the TCR, except a. combinatorial association of chains. b. combinatorial association of segments. c. large germline pool of gene sequences. d. N region addition of nucleotides. e. somatic hypermutation. 8. CD8 is a co-receptor on T cells that binds a. CD3. b. endogenous antigen peptide. c. the constant region of Class I MHC. d. the constant region of TCR. e. the variable region of Class I MHC. 9. All of the following are true for antigen receptors on both B cells and T cells EXCEPT a. associated with signal transduction molecules in the membrane. b. generated by somatic recombination during lymphocyte development. c. members of the Ig gene superfamily. d. MHC-restricted in their ability to bind antigen. e. specific for a single antigen epitope. 10. Which of the following statements is FALSE? a. TCR is allelically excluded on individual T cells. b. CD4 and CD8 co-receptors are also signal transducing molecules for T cell activation. c. The arrangement of a chain gene segments most closely resembles that of k chain. d. The gene segments for the d chain are interspersed with those for the g chain. e. The T cells that are most likely to react against allogeneic kidney cells are CD8+ cytotoxic T cells. part-9 1. Exogenous antigen includes all of the following EXCEPT a. bacterial toxins. b. extracellular protozoan parasites. c. most bacteria. d. ragweed pollen. e. viruses. 2. Human Class I MHC a chain molecules are a. b2-microglobulin. b. H-2 D, K, and L. c. H-2 IA and IE d. HLA-A. -B, and -C. e. HLA-DR, -DP, and -DQ. 3. Cells which have MHC Class II are _________________, which present _____________ antigen to Th cells. a. antigen presenting cells, endogenous b. antigen presenting cells, exogenous c. infected cells, inflammatory d. target cells, endogenous e. target cells, exogenous 4. Signaling to a cytotoxic T cell that a liver cell is infected with hepatitis virus depends on a. binding of Ii to Class I MHC until the peptide is loaded. b. binding of TCR on the cytotoxic T cell to Class II MHC on the infected cell. c. binding of processed antigen to liver cell Class I MHC. d. processing the hepatitis virus peptides to the correct size and anchor residues in the endosomal pathway. e. both c and d are correct. 5. Endogenous antigen presentation requires delivery of antigen peptides to the endoplasmic reticulum by a. Class I MHC and invariant chain. b. calnexin and tapasin. c. HLA-DM. d. leader sequence. e. TAP-1 and TAP-2. 6. Following virus infection, peptides produced from the proteasome are more likely to be presented on the surface of the target cell because a. MHC Class I is synthesized in response to virus infection. b. proteasomal enzymes which produce shorter peptides are synthesized in response to virus infection. c. TAP-1 and TAP-2 specifically bind virus peptides. d. virus amino and carboxyl terminal amino acids bind better to Class I MHC than peptides from self proteins. e. virus infection induces expression of proteases which cut proteins at sites which bind best to TAP-1 and TAP-2. 7. Exogenous antigen is processed a. after presentation by antigen presenting cells. b. by nearly every nucleated cell. c. by the cytosolic processing pathway. d. in the presence of b2-microglobulin. e. in acidified endosomes. 8. Class II MHC does not efficiently present endogenous antigen because a. antigen synthesized inside the cell never makes it to the endosomal compartment. b. endogenous antigen cannot be processed into peptides small enough. c. HLA DM transports Class II to the surface before it can bind endogenous peptide. d. invariant chain blocks binding of endogenous peptide in the ER. e. phagocytosed antigen binds Class II as rapidly as Class II is synthesized. 9. MIIC is a specialized intracellular compartment where a. HLA DM promotes the release of CLIP and peptide binding to Class II MHC. b. invariant chain binds to Class II MHC a and b chains. c. peptides are transported into the ER for binding to Class II. d. proteins are broken down into peptides by proteasomes. e. some pathogens live protected from lysosomal enzymes. 10. In order to have pathogen peptide plus Class II MHC molecules expressed on the membrane of host cells, all of the following are required EXCEPT a. b2-microglobulin. b. CLIP. c. HLA-DM. d. HLA-DR, -DP, and -DQ alpha chains. e. Ii . 11. Invariant chain (Ii) a. inhibits binding of endogenous peptide to Class I MHC. b. is degraded in the MIIC compartment to CLIP. c. is released from Class II upon binding of b2-microglobulin. d. is the constant region of Class I peptide binding site. e. prevents exogenous peptide binding to Class II MHC in the ER. 12. Antigen binding by Class I MHC molecules a. accommodates many different peptides. b. preferentially occurs for peptides 13-18 amino acids in length. c. occurs at a site on Class I MHC formed by folding of a1 and b2-microglobulin domains. d. occurs only on antigen presenting cells. e. takes place at the plasma membrane of the infected cell. 13. Both Class I and Class II MHC molecules are a. composed of a and b chains with variable and constant regions. b. expressed constitutively on all nucleated cells. c. expressed on the B cell membrane. d. part of the T cell receptor for antigen. e. synthesized in response to antigen processing. 14. The major histocompatibility complex has a. dozens of loci for Class I and Class II proteins. b. genes that encode proteins associated with antigen processing. c. only genes encoding Class I and Class II molecules. d. single loci for Class I and Class II proteins. e. three regions encoding Class I, Class II, and Class III receptors. 15. MHC polymorphism a. is generated by recombination of HLA A, B, and C gene segments. b. is present primarily in the peptide-binding regions of MHC proteins. c. is the result of random association of many alpha and beta genes. d. restricts the ability of B cells to bind antigen. e. results in expression of dozens of MHC alleles on each APC. 16. T cells are MHC-restricted in their ability to respond to antigen because a. all antigen must be processed and presented to activate lymphocytes. b. during an infection, all cells in the body present antigen on MHC Class I. c. MHC binds antigen more specifically than TCR does. d. TCR must recognize both antigen and MHC molecules. e. the T cells should not respond to antigen on allogeneic cells. 17. Linkage of a disease to an HLA allele means that a. everyone with that allele will eventually get the disease. b. people with that allele have a higher risk for the disease. c. the MHC protein encoded by that allele is defective. d. the allele will eventually disappear from the population. e. None of the above is true. 18. All of the following are associated with the expression of Class I MHC molecules EXCEPT a. antigen peptide presentation on membrane Class I MHC to Tc. b. graft rejection. c. increased risk of certain autoimmune diseases. d. lysis of virus-infected cells. e. stimulation of antibody production. 19. Human Class II MHC molecules a. are encoded by the genes HLA-A, B, and C. b. are found on all nucleated cells. c. have an antigen binding site formed from regions of two polypeptide chains. d. must be associated with b2-microglobulin molecules to bind peptide. e. present antigen to CD8 cytotoxic T cells. 20. Humans inherit from each of their parents a. a random set of MHC Class I, Class II, and Class III genes. b. enough diversity in MHC to present epitopes from most pathogens. c. enough diversity in MHC to present every possible antigen epitope. d. genes for a and b chains that can be recombined to increase their diversity. e. the same Class I and Class II MHC genes as their siblings. 21. The a chain of HLA-DR a. can be expressed with the b chain of any MHC molecule. b. can be expressed with the b chain of any Class II MHC molecule. c. can be expressed with the b chain of any Class II DR molecule. d. must be expressed with b2-microglobulin. e. must be expressed with the b chain of Class II DR from the same chromosome. 22. Which of the following statements is TRUE? a. Each individual expresses all the diversity of MHC protein structure. b. If a family has four children, no two of them will have the same MHC genotype. c. Someone with bare lymphocyte syndrome who expressed no MHC proteins would die in infancy. d. TCR on Tc cells binds a1 and b2 domains of Class I MHC protein. e. The chances of finding a tissue match are much higher between children and their parents than between siblings. 23. Which of the following statements is FALSE? a. All MHC alleles in the population have been counted. b. CD4 T cells see antigen on self Class II MHC but not on self Class I MHC. c. Human Class II MHC proteins are called HLA DP, HLA DQ, and HLA DR. d. Class I and Class II MHC are less antigen-specific than Ig. e. Peptides presented by Class I MHC must be 8-10 amino acids long. 24. Which of the following statements is FALSE? a. A peptide binding to Class I must have certain amino- and carboxyl-terminal amino acids to bind tightly to the ends of the Class I binding cleft. b. A transplant is most likely to be successful between people who share the same alleles at all Class I and Class II MHC loci. c. Identical twins share all their Class I and Class II MHC alleles. d. Peptide binding to TCR is influenced by both its own conformation and the conformation of the MHC protein to which it is bound. e. The gene for b2-microglobulin is in the Class I region of the MHC. part-10 1. An antigen binding signal at the membrane results in the mature B lymphocyte changing its a. antigen-binding specificity. b. color. c. Ig V-D-J gene rearrangement. d. gene expression. e. signal transduction molecules. 2. Signal transduction is the process of converting a. a B cell to a T cell. b. a binding signal to a chemical signal. c. a hapten to an antigen. d. IgA to secretory IgA. e. a kinase to a phosphatase. 3. A ligand is a. a cytokine. b. a molecule that specifically binds a receptor. c. an antigen. d. an enzyme. e. all of the above are ligands. 4. A tyrosine kinase which is activated by antigen binding is found in the __________ of the BCr or TCR complex. a. cytoplasmic domain b. extracellular domain. c. Ig superfamily domain. d. transmembrane domain. e. variable domain. 5. The ligand for TCR is a. BCR. b. MHC c. MHC + peptide. d. peptide. e. TCR ligand. 6. An oncogene is a gene that is associated with a. apoptosis. b. cancer. c. ITIMs. d. TCR and BCR signal transduction. e. viruses. 7. Antigen binding to B cells is most effective at sending an activation signal to the B cell if it causes a. antigen processing and presentation on Class II MHC. b. BCR clustering. c. BCR internalization. d. inflammation. e. opsonization. 8. An enzyme which puts a phosphate group on a protein molecule is called a a. co-receptor. b. ITAM. c. kinase. d. phosphatase. e. receptor. 9. Gene expression does NOT necessarily involve a. changes in a cell's activities (phenotype). b. mRNA synthesis. c. protein synthesis. d. DNA synthesis. e. transcription factors. 10. The signal transduction molecules associated with TCR are a. CD1. b. CD3. c. CD4. d. CD8. e. CD22. 11. The signal transduction molecules associated with BCR are a. CD21 and CD81. b. Iga and Igb c. IgD and IgM. d. ITAMs and ITIMs. e. RAG-1 and RAG-2. 12. The second messenger IP3 increases the cytoplasmic concentration of a. antigen. b. calcium. c. Class I MHC. d. phosphate. e. sodium. 13. DAG and IP3 are released from PIP2 by the action of a. adaptor protein. b. phospholipase C (PLC). c. protein kinase C (PKC). d. small G protein. e. TdT. 14. Small G proteins (like Ras) convert GTP to GDP by their ___________ activity. a. GEF. b. kinase. c. phosphatase. d. polymerase. e. protease. 15. Transcription factors a. increase synthesis of mRNA. b. increase synthesis of DNA. c. inhibit synthesis of mRNA. d. promote DNA phosphorylation. e. synthesize mRNA. 16. An enzyme cascade is a a. case where the enzyme catalyzes its own inactivation, like small G proteins. b. pair of enzymatic reactions that have opposite effects, like kinases and phosphatases. c. series of enzymatic reactions that result in cancer. d. series of enzymatic reactions where the product of one reaction catalyzes the next reaction. e. small waterfall. 17. Signal transduction complex associates with TCR in the membrane through a. agonist peptides. b. covalent bonds. c. enzyme cascades. d. reverse phosphorylation. e. salt bridges. 18. If IgaIgb cannot be made, B cells a. cannot express BCR. b. cannot express Class II MHC. c. express 1,000-fold less BCR than usual d. synthesize CD3 and become T cells. e. require 1,000-fold more antigen to be activated. 19. The immune system of a person who had a mutation in CD3 could NOT fight a viral hepatitis A infection by a. blocking Hepatitis A virus from infecting liver cells with neutralizing IgG antibodies. b. generating cytotoxic T cells to lyse infected liver cells c. lysing virus-infected cells with NK cells. d. phagocytosing complement-opsonized Hepatitis A virus. e. Both 1 and 2 are correct. 20. Amino acid sequences in lymphocyte signal transduction complexes which are phosphorylated following antigen binding are called a. ITAMs. b. ITIMs. c. MAPs. d. PTKs. e. syks. 21. An immune deficiency resulting from a defective PTK in the activation cascade in B cells would probably be characterized by a. high numbers of circulating B cells. b. high numbers of circulating lymphocytes. c. high concentrations of plasma immunoglobulins. d. low concentrations of plasma immunoglobulins. e. low numbers of circulating T cells. 22. B cell co-receptor complex CD19, CD22, and CD81 a. allows B cells to be activated with 1,000-fold less complement-coated antigen. b. allows B cells to be activated with 1,000-fold more complement-coated antigen. c. decreases B cell expression of BCR. d. increases B cell expression of BCR. e. prevents B cell activation by self antigen. 23. The anti-rejection drugs cyclosporin A and FK506 block rejection of transplanted organs by interfering with a. activation of a T cell transcription factor required for T cell activation. b. antibody synthesis required for ADCC of transplanted cells. c. CD3 expression. d. MHC Class I expression. e. processing of graft peptides and presentation on Class I MHC. 24. Antagonist peptides a. fail to bind to T cells. b. fully activate T cells. c. interfere with T cell activation by agonist peptides. d. partially activate T cells. e. require partial agonist peptides to fully activate T cells. 25. Antibody-dependent cell-mediated cytotoxicity (ADCC) is a process in which antibody-coated cells are killed by a. the antibodies. b. complement. c. cytotoxic T cells. d. cells with Fc receptors for IgG3. e. cells with Fc receptors for IgE. 26. When IgE on mast cell FceR is cross-linked by, antigen, the mast cell responds by a. apoptosis. b. presenting the antigen to Th cells. c. secreting IgE. d. secreting histamine and other allergic mediators. e. stimulating macrophage and neutrophil phagocytosis of the coated antigen. 27. Homeostasis is a. macrophage activation by bacterial antigens. b. programmed cell death. c. the normal process of signal transduction. d. the synthesis from all leukocytes from bone marrow stem cells. e. the regulation of biological systems within normal limits. 28. STAT proteins are NOT a. cytosolic proteins. b. involved in cytokine signaling. c. JAK kinases. d. signal transducers. e. transcription activators. 29. Cells receive a death signal through a. bcl-2 receptor. b. death receptor. c. Fas. d. Fas ligand. e. STAT ligand. 30. The most important receptor through which lymphocytes receive life and death signals is a. antigen receptor. b. bcl-2 receptor. c. Fas receptor. d. FcR. e. growth factor receptor.