UCLA MIMG C185A FINAL EXAM STUDY
GUIDE QUESTIONS, ANSWERS AND
RATIONALES (LATEST 2026 UPDATE)
This premium 2026 study guide provides a comprehensive
repository of verified, high-yield multiple-choice questions
with detailed rationales covering core molecular
immunology concepts at UCLA. It tracks lymphocyte
development pathways, receptor recombination
mechanisms, and clinical immunopathology scenarios to
mirror the exact structural layout of the final exam.
Mastering these targeted problem sets offers students an
efficient path toward achieving top marks on their
cumulative assessments.
Q1. A genetic knockout mouse completely lacks expression of the λ5
(Lambda 5) protein. At which specific stage will B-cell development be
entirely arrested?
A) Early Pro-B cell stage
B) Pre-B cell stage
,C) Immature B cell stage
D) Mature naive B cell stage
Answer: B
Rationale: λ5 is a critical structural component of the surrogate light
chain (SLC). Along with VpreB, it forms the pre-B cell receptor (pre-
BCR) complex paired with the rearranged μ heavy chain. Without λ5,
the pre-BCR cannot assemble or signal, halting development abruptly
at the transition from the Pro-B to the Pre-B cell stage.
Q2. During a laboratory experiment, a T cell successfully recognizes
an antigen presented on an APC, but the APC lacks B7-1 (CD80) or
B7-2 (CD86) surface expression. What is the immediate functional
outcome for this T cell?
A) Clonal expansion and differentiation
B) Immediate upregulation of CD40L
C) Cellular anergy or apoptosis
D) Hyper-responsiveness to subsequent encounters
Answer: C
Rationale: T-cell activation requires two distinct signals. Signal 1 is
the TCR binding to the peptide-MHC complex. Signal 2 is the co-
stimulatory signal provided by the binding of CD28 on the T cell to
B7-1/B7-2 on the APC. In the absence of Signal 2, the T cell enters a
state of metabolic and functional unresponsiveness known as clonal
anergy, or it undergoes programmed cell death (apoptosis).
Q3. A patient presents with a rare genetic mutation that prevents the
transcription of the Iε region upstream of the heavy-chain constant
genes. Which antibody isotype will this patient be completely unable
to produce?
A) IgG1
B) IgA
,C) IgE
D) IgM
Answer: C
Rationale: Class switch recombination (CSR) is guided by cytokine-
induced transcription through specific switch (S) regions located
upstream of heavy-chain constant (\(C_{H}\)) genes. The Iε promoter
and exon control transcription through the Sε region. When
Interleukin-4 (IL-4) stimulates this locus, it opens the chromatin for
access. If transcription of the Iε region is blocked, the cell cannot
undergo CSR to IgE.
Q4. Which of the following enzymes is directly responsible for
introducing double-stranded DNA breaks into switch (S) regions
during antibody class switch recombination?
A) RAG-1
B) RAG-2
C) Terminal Deoxynucleotidyl Transferase (TdT)
D) Activation-Induced Cytidine Deaminase (AID)
Answer: D
Rationale: Activation-Induced Cytidine Deaminase (AID) deaminates
cytosine residues to uracil within single-stranded target DNA tracks
during transcription. The resulting uracils are removed by uracil-DNA
glycosylase (UNG), and the apyrimidinic sites are cleaved by AP
endonuclease, leading to targeted single- and double-stranded DNA
breaks within the switch (S) regions necessary for class switching.
Q5. A severe immunodeficiency is traced back to a null mutation in
both the RAG-1 and RAG-2 genes. Which cellular phenotype is
expected in the peripheral blood of this patient?
A) Absence of B cells but normal numbers of T cells
B) Absence of T cells but normal numbers of B cells
, C) Complete absence of both mature B cells and mature T cells
D) Elevated levels of hyper-mutated IgM antibodies
Answer: C
Rationale: Recombination-Activating Genes 1 and 2 (RAG-1/2) code
for the lymphoid-specific endonuclease complex that recognizes
Recombination Signal Sequences (RSS). This complex is strictly
required to execute somatic V(D)J recombination. Without functional
RAG proteins, neither B-cell receptors (immunoglobulins) nor T-cell
receptors (TCRs) can assemble their variable regions, resulting in an
absolute developmental block for both lineages.
Q6. What is the fundamental, central protein of the complement
cascade where the alternative, classical, and lectin pathways all
converge?
A) C1q
B) C3
C) C5
D) C9
Answer: B
Rationale: While the initiation steps differ among the three
complement arms, all pathways culminate in the formation of a C3
convertase enzyme. The cleavage of C3 into C3a (anaphylatoxin) and
C3b (opsonin/convertase component) represents the critical, central
amplification step of the entire complement cascade.
Q7. In an in vitro assay, pro-B cells are isolated from an Ig-α (CD79a)
knockout mouse. What will be the observed surface expression
phenotype of these cells upon heavy chain rearrangement?
A) High levels of surface IgM expression
B) Normal pre-BCR assembly but no intracellular signaling
C) Complete failure to transport the rearranged heavy chain to the cell
GUIDE QUESTIONS, ANSWERS AND
RATIONALES (LATEST 2026 UPDATE)
This premium 2026 study guide provides a comprehensive
repository of verified, high-yield multiple-choice questions
with detailed rationales covering core molecular
immunology concepts at UCLA. It tracks lymphocyte
development pathways, receptor recombination
mechanisms, and clinical immunopathology scenarios to
mirror the exact structural layout of the final exam.
Mastering these targeted problem sets offers students an
efficient path toward achieving top marks on their
cumulative assessments.
Q1. A genetic knockout mouse completely lacks expression of the λ5
(Lambda 5) protein. At which specific stage will B-cell development be
entirely arrested?
A) Early Pro-B cell stage
B) Pre-B cell stage
,C) Immature B cell stage
D) Mature naive B cell stage
Answer: B
Rationale: λ5 is a critical structural component of the surrogate light
chain (SLC). Along with VpreB, it forms the pre-B cell receptor (pre-
BCR) complex paired with the rearranged μ heavy chain. Without λ5,
the pre-BCR cannot assemble or signal, halting development abruptly
at the transition from the Pro-B to the Pre-B cell stage.
Q2. During a laboratory experiment, a T cell successfully recognizes
an antigen presented on an APC, but the APC lacks B7-1 (CD80) or
B7-2 (CD86) surface expression. What is the immediate functional
outcome for this T cell?
A) Clonal expansion and differentiation
B) Immediate upregulation of CD40L
C) Cellular anergy or apoptosis
D) Hyper-responsiveness to subsequent encounters
Answer: C
Rationale: T-cell activation requires two distinct signals. Signal 1 is
the TCR binding to the peptide-MHC complex. Signal 2 is the co-
stimulatory signal provided by the binding of CD28 on the T cell to
B7-1/B7-2 on the APC. In the absence of Signal 2, the T cell enters a
state of metabolic and functional unresponsiveness known as clonal
anergy, or it undergoes programmed cell death (apoptosis).
Q3. A patient presents with a rare genetic mutation that prevents the
transcription of the Iε region upstream of the heavy-chain constant
genes. Which antibody isotype will this patient be completely unable
to produce?
A) IgG1
B) IgA
,C) IgE
D) IgM
Answer: C
Rationale: Class switch recombination (CSR) is guided by cytokine-
induced transcription through specific switch (S) regions located
upstream of heavy-chain constant (\(C_{H}\)) genes. The Iε promoter
and exon control transcription through the Sε region. When
Interleukin-4 (IL-4) stimulates this locus, it opens the chromatin for
access. If transcription of the Iε region is blocked, the cell cannot
undergo CSR to IgE.
Q4. Which of the following enzymes is directly responsible for
introducing double-stranded DNA breaks into switch (S) regions
during antibody class switch recombination?
A) RAG-1
B) RAG-2
C) Terminal Deoxynucleotidyl Transferase (TdT)
D) Activation-Induced Cytidine Deaminase (AID)
Answer: D
Rationale: Activation-Induced Cytidine Deaminase (AID) deaminates
cytosine residues to uracil within single-stranded target DNA tracks
during transcription. The resulting uracils are removed by uracil-DNA
glycosylase (UNG), and the apyrimidinic sites are cleaved by AP
endonuclease, leading to targeted single- and double-stranded DNA
breaks within the switch (S) regions necessary for class switching.
Q5. A severe immunodeficiency is traced back to a null mutation in
both the RAG-1 and RAG-2 genes. Which cellular phenotype is
expected in the peripheral blood of this patient?
A) Absence of B cells but normal numbers of T cells
B) Absence of T cells but normal numbers of B cells
, C) Complete absence of both mature B cells and mature T cells
D) Elevated levels of hyper-mutated IgM antibodies
Answer: C
Rationale: Recombination-Activating Genes 1 and 2 (RAG-1/2) code
for the lymphoid-specific endonuclease complex that recognizes
Recombination Signal Sequences (RSS). This complex is strictly
required to execute somatic V(D)J recombination. Without functional
RAG proteins, neither B-cell receptors (immunoglobulins) nor T-cell
receptors (TCRs) can assemble their variable regions, resulting in an
absolute developmental block for both lineages.
Q6. What is the fundamental, central protein of the complement
cascade where the alternative, classical, and lectin pathways all
converge?
A) C1q
B) C3
C) C5
D) C9
Answer: B
Rationale: While the initiation steps differ among the three
complement arms, all pathways culminate in the formation of a C3
convertase enzyme. The cleavage of C3 into C3a (anaphylatoxin) and
C3b (opsonin/convertase component) represents the critical, central
amplification step of the entire complement cascade.
Q7. In an in vitro assay, pro-B cells are isolated from an Ig-α (CD79a)
knockout mouse. What will be the observed surface expression
phenotype of these cells upon heavy chain rearrangement?
A) High levels of surface IgM expression
B) Normal pre-BCR assembly but no intracellular signaling
C) Complete failure to transport the rearranged heavy chain to the cell
