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PCB 3233 Immunology EXAM 2 STUDY GUIDE 2026 COMPLETE QUESTIONS WITH CORRECT DETAILED ANSWERS || 100% GUARANTEED PASS LATEST VERSION

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PCB 3233 Immunology EXAM 2 STUDY GUIDE 2026 COMPLETE QUESTIONS WITH CORRECT DETAILED ANSWERS || 100% GUARANTEED PASS LATEST VERSION

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PCB 3233 Immunology EXAM 2 STUDY GUIDE
2026 COMPLETE QUESTIONS WITH CORRECT
DETAILED ANSWERS || 100% GUARANTEED
PASS <LATEST VERSION>
PCB 3233 Immunology Exam 2 Study Guide

100 Questions with Detailed Answers

Section 1: Antigen Recognition & B Cell Receptors

1. Q: What are the two primary forms of immunoglobulin (Ig) expressed by B cells, and
what are their functions?
A: Membrane-bound Ig (BCR) for antigen recognition and signal initiation; secreted Ig
(antibody) for effector functions like neutralization and opsonization.

2. Q: What genetic rearrangement processes create the diversity of the B cell receptor?
A: V(D)J recombination of variable (V), diversity (D), and joining (J) gene segments for
heavy chain, and V-J recombination for light chain.

3. Q: What enzyme complex is essential for V(D)J recombination?
A: RAG-1/RAG-2 (Recombination Activating Genes).

4. Q: What is allelic exclusion and why is it important?
A: Ensures each B cell expresses only one specific BCR by inhibiting rearrangement of the
second allele after successful rearrangement of the first.

5. Q: What is the difference between a naïve B cell and a plasma cell in terms of
immunoglobulin expression?
A: Naïve B cells express membrane-bound IgM and IgD; plasma cells secrete large
amounts of antibody (IgG, IgA, or IgE) and no longer express membrane Ig.

Section 2: T Cell Receptors & MHC

6. Q: What is the structure of the αβ T cell receptor?
A: A heterodimer composed of an α chain and a β chain, each with a variable and
constant region, associated with CD3 signaling complexes.

, 7. Q: How does TCR diversity generation differ from BCR generation?
A: TCRs undergo V(D)J recombination but do not undergo somatic hypermutation or
class switching after antigen exposure.

8. Q: What are the two main classes of MHC molecules and which cells express them?
A: Class I MHC (expressed on all nucleated cells); Class II MHC (expressed on professional
antigen-presenting cells: dendritic cells, macrophages, B cells).

9. Q: Which T cell subset recognizes peptide antigen presented by MHC Class I vs. Class
II?
A: CD8+ cytotoxic T cells recognize peptide + MHC I; CD4+ helper T cells recognize
peptide + MHC II.

10. Q: What is cross-presentation and why is it critical for antiviral immunity?
A: The process where dendritic cells present exogenous viral antigens on MHC Class I to
activate CD8+ T cells.

Section 3: Antigen Presentation & Processing

11. Q: Describe the endogenous antigen processing pathway for MHC Class I presentation.
A: Cytosolic proteins are degraded by the proteasome, transported into the ER via TAP,
loaded onto MHC I with help from chaperones, then transported to the cell surface.


12. Q: Describe the exogenous antigen processing pathway for MHC Class II presentation.
A: Extracellular proteins are endocytosed, degraded in acidic endosomes/lysosomes.
MHC II is stabilized by invariant chain (Ii) in ER, then peptide loading occurs in MHC II
compartment (MIIC) after Ii removal.

13. Q: What is the role of HLA-DM?
A: Facilitates the removal of CLIP from MHC II and stabilizes empty MHC II to allow
binding of higher affinity peptides.

14. Q: What is the immunological consequence of a deficiency in TAP proteins?
A: Greatly reduced surface MHC Class I expression, leading to impaired CD8+ T cell
responses and susceptibility to viral infections.

Section 4: B Cell Activation & Germinal Center Reactions

15. Q: What two signals are required for naïve B cell activation by a protein antigen?
A: Signal 1: Antigen cross-linking of BCR. Signal 2: Co-stimulation from helper T cells
(CD40L on T cell binding CD40 on B cell + cytokines).

, 16. Q: Where do primary B cell activation and the germinal center reaction occur?
A: Primary activation at the T cell-B cell border in secondary lymphoid organs; germinal
center reaction within lymphoid follicles.

17. Q: What are the three major fates of B cells within the germinal center?
A: Somatic hypermutation & affinity maturation, class switch recombination,
differentiation into memory B cells or plasma cells.

18. Q: What is somatic hypermutation (SHM) and which enzyme mediates it?
A: Introduction of point mutations in the variable regions of immunoglobulin genes;
mediated by Activation-Induced Cytidine Deaminase (AID).

19. Q: What is the mechanism of class switch recombination (CSR)?
A: AID mediates DNA breaks at switch regions upstream of constant genes, allowing
recombination to a downstream constant region (e.g., from Cμ to Cγ), changing antibody
isotype (e.g., IgM to IgG).

Section 5: T Cell Activation & Differentiation

20. Q: What are the three signals required for full naïve T cell activation?
A: 1. TCR-pMHC interaction. 2. Co-stimulation (CD28:B7). 3. Cytokines for differentiation.


21. Q: What is the consequence of Signal 1 (TCR) without Signal 2 (co-stimulation)?
A: Leads to T cell anergy (unresponsiveness) or deletion.

22. Q: What transcription factor is the "master regulator" for Treg cell development and
function?
A: FoxP3.

23. Q: What cytokine drives Th1 differentiation, and what is the key transcription factor?
A: IL-12 and IFN-γ drive Th1 differentiation; T-bet is the master transcription factor.


24. Q: What cytokine drives Th2 differentiation, and what is the key transcription factor?
A: IL-4 drives Th2 differentiation; GATA3 is the master transcription factor.

25. Q: What cytokines drive Th17 differentiation?
A: TGF-β plus IL-6 or IL-21; RORγt is the key transcription factor.

26. Q: What is the primary function of T follicular helper (Tfh) cells?
A: To provide help to B cells in germinal centers for affinity maturation and class
switching (express CXCR5, PD-1, secrete IL-21).

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