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17 BMD 430 lecture 17

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

B. Slow response, mainly IgM antibodies first

2.

2. During the secondary immune response, the predominant antibody type is:
A. IgM
B. IgA
C. IgG
D. IgD

C. IgG

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

B. Memory cells already exist and have higher affinity receptors

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

C. Circulate and can re-enter germinal centers upon re-exposure

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

B. Inhibit B cell activation to prevent overreaction

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

B. Rh− mother has an Rh+ baby and develops antibodies against fetal RBCs

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

C. Destroying fetal Rh+ cells before the mother’s immune system can react

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

C. Naïve T cells express CD45RA; memory T cells express CD45RO

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

C. Tissue-resident memory (Trm)

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

C. A combination of both early and effector-derived memory cells

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

B. The immune system reuses old memory responses even to mutated viruses

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

C. It has a high mutation rate, leading to mismatched immune memory

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

B. Antibodies recognizing structurally similar antigens

14.

14. Cross-protection provides:
A. Temporary protection against related pathogens
B. Immediate full immunity
C. No benefit across infections
D. Autoimmune disease

A. Temporary protection against related pathogens

15.

Explain the key timeline difference between primary and secondary immune responses.

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.

16.

Describe how the DNA-level changes differ between primary and secondary responses.

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.

17.

List the major cell types involved in immunological memory

Memory B cells, long-lived plasma cells, and memory T cells (CD4⁺ and CD8⁺).

18.

Compare long-lived plasma cells and memory B cells.

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.

19.

What is the function of FcγR2B(1)?

It is an inhibitory receptor on B cells that prevents overactivation, maintaining immune balance and preventing autoimmunity.

20.

Explain the cause and mechanism of erythroblastosis fetalis.

Occurs when an Rh− mother produces anti-Rh antibodies after carrying an Rh+ baby; in a later Rh+ pregnancy, these antibodies attack fetal RBCs.

21.

How does Rhogam prevent hemolytic disease of the newborn?

Rhogam (anti-Rh antibodies) destroys fetal Rh+ cells before the mother’s immune system can detect and react to them.

22.

What is the difference between CD45RA and CD45RO?

CD45RA is expressed on naïve T cells; CD45RO is on memory T cells. Structural changes from splicing make memory T cells respond faster.

23.

Name the three types of memory T cells and describe their migration patterns

  • Tcm: Stay in lymph nodes.
  • Tem: Circulate in blood and tissues.
  • Trm: Reside in specific tissues for local defense.
24.

Define original antigenic sin and its significance.

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.

25.

Why is cross-reactivity important?

It allows antibodies to recognize and partially protect against similar pathogens, leading to cross-protection between related strains.

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.

C. Memory B and T cells respond rapidly with high-affinity receptors.

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

B. Maternal memory B cells will attack fetal red blood cells.

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.

B. Long-lived plasma and memory T cells provide rapid immunity.

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

C. Increased risk of autoimmune reactions

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

B. Cross-reactivity and cross-protection

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.

C. The second exposure produces mainly IgG antibodies more quickly.

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

C. Tissue-resident memory (Trm)

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

B. Original antigenic sin

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.

C. Both models occur, depending on the immune environment.

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.

B. Group B are memory T cells that respond faster due to altered CD45 signaling.