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17 BMD 430 lecture 17

front 1 1. Which of the following correctly describes the primary immune response? A. Rapid response with mainly IgG antibodies B. Slow response, mainly IgM antibodies first C. Requires memory cells from a previous exposure D. Occurs faster due to affinity-matured B cells	back 1 B. Slow response, mainly IgM antibodies first
front 2 2. During the secondary immune response, the predominant antibody type is: A. IgM B. IgA C. IgG D. IgD	back 2 C. IgG
front 3 3. Which statement best explains why the secondary immune response is faster? A. Naïve cells divide faster B. Memory cells already exist and have higher affinity receptors C. New somatic mutations occur immediately D. Antigens are smaller and easier to detect	back 3 B. Memory cells already exist and have higher affinity receptors
front 4 4. Memory B cells differ from long-lived plasma cells in that memory B cells: A. Continuously secrete antibodies B. Are terminally differentiated C. Circulate and can re-enter germinal centers upon re-exposure D. Are only found in bone marrow	back 4 C. Circulate and can re-enter germinal centers upon re-exposure

front 5 5. The FcγR2B(1) receptor on B cells functions to: A. Activate B cells and increase antibody secretion B. Inhibit B cell activation to prevent overreaction C. Promote antibody isotype switching D. Stimulate plasma cell differentiation	back 5 B. Inhibit B cell activation to prevent overreaction
front 6 6. Hemolytic disease of the newborn occurs when: A. Rh+ mother has an Rh− baby B. Rh− mother has an Rh+ baby and develops antibodies against fetal RBCs C. Rh− mother has an Rh− baby D. Rh+ father and Rh+ mother produce Rh− baby	back 6 B. Rh− mother has an Rh+ baby and develops antibodies against fetal RBCs
front 7 7. Rhogam prevents erythroblastosis fetalis by: A. Stimulating antibody production in the mother B. Blocking fetal Rh receptors C. Destroying fetal Rh+ cells before the mother’s immune system can react D. Neutralizing maternal anti-Rh antibodies	back 7 C. Destroying fetal Rh+ cells before the mother’s immune system can react
front 8 8. Which of the following distinguishes naïve from memory T cells? A. Naïve T cells express CD45RO B. Memory T cells express CD45RA C. Naïve T cells express CD45RA; memory T cells express CD45RO D. Both express the same CD45 isoform	back 8 C. Naïve T cells express CD45RA; memory T cells express CD45RO

front 9 9. Which memory T cell type primarily remains in tissues such as skin, gut, and lungs? A. Effector memory (Tem) B. Central memory (Tcm) C. Tissue-resident memory (Trm) D. Naïve T cells	back 9 C. Tissue-resident memory (Trm)
front 10 10. Which model of memory cell differentiation is currently considered most accurate? A. Only effector cells can become memory cells B. Only early progenitors form memory cells C. A combination of both early and effector-derived memory cells D. Memory cells arise from plasma cells only	back 10 C. A combination of both early and effector-derived memory cells
front 11 11. The concept of original antigenic sin explains that: A. The immune system always produces new antibodies for each new strain B. The immune system reuses old memory responses even to mutated viruses C. The immune system forgets previous infections D. Antibodies mutate faster than viruses	back 11 B. The immune system reuses old memory responses even to mutated viruses
front 12 12. Why is influenza a good example of original antigenic sin? A. It never mutates B. Its antibodies are very stable C. It has a high mutation rate, leading to mismatched immune memory D. It only infects once	back 12 C. It has a high mutation rate, leading to mismatched immune memory

front 13 13. Cross-reactivity leads to: A. Immune response against completely unrelated antigens B. Antibodies recognizing structurally similar antigens C. No immune response to related pathogens D. Complete protection from all viruses	back 13 B. Antibodies recognizing structurally similar antigens
front 14 14. Cross-protection provides: A. Temporary protection against related pathogens B. Immediate full immunity C. No benefit across infections D. Autoimmune disease	back 14 A. Temporary protection against related pathogens
front 15 Explain the key timeline difference between primary and secondary immune responses.	back 15 Primary responses are slower (7–10 days) and mainly produce IgM, while secondary responses occur faster (1–3 days) and mainly produce IgG with higher affinity and longer duration.
front 16 Describe how the DNA-level changes differ between primary and secondary responses.	back 16 In the primary response, somatic hypermutation and class switching occur slowly for the first time. In the secondary response, B cells already have rearranged, high-affinity DNA, allowing quick antibody production.

front 17 List the major cell types involved in immunological memory	back 17 Memory B cells, long-lived plasma cells, and memory T cells (CD4⁺ and CD8⁺).
front 18 Compare long-lived plasma cells and memory B cells.	back 18 Plasma cells live in bone marrow and constantly secrete antibodies but do not divide. Memory B cells circulate and wait for reactivation; they don’t secrete antibodies until stimulated.
front 19 What is the function of FcγR2B(1)?	back 19 It is an inhibitory receptor on B cells that prevents overactivation, maintaining immune balance and preventing autoimmunity.
front 20 Explain the cause and mechanism of erythroblastosis fetalis.	back 20 Occurs when an Rh− mother produces anti-Rh antibodies after carrying an Rh+ baby; in a later Rh+ pregnancy, these antibodies attack fetal RBCs.

front 21 How does Rhogam prevent hemolytic disease of the newborn?	back 21 Rhogam (anti-Rh antibodies) destroys fetal Rh+ cells before the mother’s immune system can detect and react to them.
front 22 What is the difference between CD45RA and CD45RO?	back 22 CD45RA is expressed on naïve T cells; CD45RO is on memory T cells. Structural changes from splicing make memory T cells respond faster.
front 23 Name the three types of memory T cells and describe their migration patterns	back 23 Tcm: Stay in lymph nodes. Tem: Circulate in blood and tissues. Trm: Reside in specific tissues for local defense.
front 24 Define original antigenic sin and its significance.	back 24 It is when the immune system relies on old antibodies from a previous infection, even if a new strain has mutated. This can reduce the effectiveness of the immune response.

front 25 Why is cross-reactivity important?	back 25 It allows antibodies to recognize and partially protect against similar pathogens, leading to cross-protection between related strains.
front 26 1. A child receives their second MMR vaccine dose and produces antibodies faster than after the first dose. What explains this? A. The child’s immune system has more naïve B cells. B. The second vaccine causes stronger inflammation. C. Memory B and T cells respond rapidly with high-affinity receptors. D. The vaccine is more concentrated.	back 26 C. Memory B and T cells respond rapidly with high-affinity receptors.
front 27 2. A pregnant Rh− woman who never received Rhogam after her first Rh+ pregnancy is now carrying another Rh+ baby. What is likely to occur? A. The baby will produce anti-Rh antibodies. B. Maternal memory B cells will attack fetal red blood cells. C. The baby’s immune system will reject maternal antibodies. D. The mother will be protected by Rhogam	back 27 B. Maternal memory B cells will attack fetal red blood cells.
front 28 3. A nurse who had chickenpox as a child is exposed to shingles but does not become ill. What best explains her protection? A. Naïve B cells immediately produce IgM. B. Long-lived plasma and memory T cells provide rapid immunity. C. She has innate resistance to herpesviruses. D. The exposure dose was too low to infect her.	back 28 B. Long-lived plasma and memory T cells provide rapid immunity.

front 29 4. A patient has a genetic defect in the FcγR2B(1) receptor. Which immune issue might they experience? A. Impaired antibody production B. Reduced T cell activation C. Increased risk of autoimmune reactions D. Weakened complement activation	back 29 C. Increased risk of autoimmune reactions
front 30 5. After receiving a flu vaccine, a patient becomes infected with a slightly different strain but has only mild symptoms. Which concepts explain this? A. Antigenic drift and original antigenic sin B. Cross-reactivity and cross-protection C. Autoimmunity and tolerance D. Antigenic variation and suppression	back 30 B. Cross-reactivity and cross-protection
front 31 6. Two mice are studied: one exposed to a virus for the first time, and one exposed twice. Which statement is true? A. Both mice produce mostly IgM in equal amounts. B. The first exposure causes a faster response. C. The second exposure produces mainly IgG antibodies more quickly. D. The second exposure produces fewer antibodies overall.	back 31 C. The second exposure produces mainly IgG antibodies more quickly.
front 32 7. During a viral infection, a memory T cell in the skin releases cytokines immediately without returning to lymph nodes. What type of memory T cell is this? A. Central memory (Tcm) B. Effector memory (Tem) C. Tissue-resident memory (Trm) D. Naïve T cell	back 32 C. Tissue-resident memory (Trm)

front 33 8. Researchers find that people exposed to an old flu strain respond poorly to a new, mutated strain. What does this illustrate? A. Cross-protection B. Original antigenic sin C. Antigenic drift D. Clonal deletion	back 33 B. Original antigenic sin
front 34 9. Two patients develop memory cells differently: one forms them early, and the other from surviving effector cells. What conclusion is correct? A. Only early formation is possible. B. Only effector survival can produce memory. C. Both models occur, depending on the immune environment. D. Neither model is accurate.	back 34 C. Both models occur, depending on the immune environment.
front 35 10. A researcher studies two T cell groups. Group A expresses CD45RA, while Group B expresses CD45RO. Which statement is correct? A. Group A are memory T cells; Group B are naïve. B. Group B are memory T cells that respond faster due to altered CD45 signaling. C. Both groups are naïve but differ in cytokine production. D. Group A cells are effector memory cells.	back 35 B. Group B are memory T cells that respond faster due to altered CD45 signaling.