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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 15. Which statement best describes the key timeline difference between primary and secondary immune responses? A. Primary is faster and produces IgG; secondary is slower and produces IgM B. Primary is slow (7–10 days, mainly IgM); secondary is fast (1–3 days, mainly IgG) C. Both occur at the same speed but differ in antibody type D. Secondary responses occur only after vaccination	back 15 B. Primary is slow (7–10 days, mainly IgM); secondary is fast (1–3 days, mainly IgG)
front 16 16. How do DNA-level changes differ between primary and secondary immune responses? A. Secondary responses require new class-switch recombination B. Primary responses use pre-mutated DNA from memory cells C. Primary responses perform SHM and class switching for the first time; secondary responses use pre-mutated, high-affinity DNA D. DNA changes do not differ between the two	back 16 C. Primary responses perform SHM and class switching for the first time; secondary responses use pre-mutated, high-affinity DNA.

front 17 17. Which of the following lists the major cell types involved in immunological memory? A. Mast cells, NK cells, neutrophils B. Memory B cells, long-lived plasma cells, memory T cells C. Macrophages, dendritic cells, eosinophils D. Th17 cells only	back 17 B. Memory B cells, long-lived plasma cells, memory T cells
front 18 18. Which statement correctly compares long-lived plasma cells and memory B cells? A. Plasma cells circulate; memory B cells stay in bone marrow B. Plasma cells divide frequently; memory B cells never divide C. Plasma cells secrete antibodies continuously; memory B cells wait for reactivation D. Memory B cells secrete antibodies constitutively	back 18 C. Plasma cells secrete antibodies continuously; memory B cells wait for reactivation
front 19 19. What is the role of FcγR2B(1) on B cells? A. Enhances B-cell activation B. Functions as an inhibitory receptor to prevent overactivation C. Triggers complement activation D. Activates macrophages	back 19 B. Functions as an inhibitory receptor to prevent overactivation
front 20 20. What causes erythroblastosis fetalis (hemolytic disease of the newborn)? A. ABO incompatibility between mother and fetus B. Rh− mother makes anti-Rh antibodies that attack a later Rh+ fetus C. Excess maternal IgA crosses the placenta D. Fetal T cells attack maternal RBCs	back 20 B. Rh− mother makes anti-Rh antibodies that attack a later Rh+ fetus

front 21 21. How does Rhogam prevent hemolytic disease of the newborn? A. By blocking maternal IgG from crossing the placenta B. By suppressing fetal antigen expression C. By destroying fetal Rh+ RBCs before the mother can recognize them D. By increasing maternal T-cell tolerance	back 21 C. By destroying fetal Rh+ RBCs before the mother can recognize them
front 22 22. What is the difference between CD45RA and CD45RO? A. CD45RO is on naïve T cells; CD45RA on memory T cells B. CD45RA on naïve T cells; CD45RO on memory T cells, allowing faster responses C. CD45RA is a B-cell marker; CD45RO is a macrophage marker D. They are identical splice variants	back 22 B. CD45RA on naïve T cells; CD45RO on memory T cells, allowing faster responses
front 23 23. Which of the following correctly describes the migration patterns of the three types of memory T cells? A. Tcm in blood; Tem in lymph nodes; Trm in bone marrow B. Tcm in tissues; Tem only in lymph nodes; Trm circulate widely C. Tcm in lymph nodes; Tem circulate in blood and tissues; Trm reside permanently in tissues D. All memory T cells circulate freely everywhere	back 23 C. Tcm in lymph nodes; Tem circulate in blood and tissues; Trm reside permanently in tissues
front 24 24. What is original antigenic sin? A. When a pathogen mutates to evade T cells B. When the immune system responds only with innate immunity C. Preferential use of old antibodies from a prior strain, even if the new strain is different D. Failure to produce antibodies after vaccination	back 24 C. Preferential use of old antibodies from a prior strain, even if the new strain is different

front 25 Why is cross-reactivity important? A. It causes autoimmunity B. It allows antibodies to recognize similar pathogens and provide partial protection C. It prevents memory B-cell formation D. It blocks antibody production	back 25 B. It allows antibodies to recognize similar pathogens and provide partial protection
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.