PCB 3233 | PCB3233 Exam 4: Immunology -
University of Central Florida Updated and Latest
Questions and Correct Answers with Rationale
1. A 25-year-old patient presents with sudden onset of wheezing, hives, and hypotension
after a bee sting. Which immunological mechanism is primarily responsible for this
immediate reaction?
A. IgG-mediated cytotoxic cell lysis
B. T-cell mediated delayed hypersensitivity
C. Immune complex deposition in small vessels
D. IgE-mediated mast cell degranulation
Correct Answer: D
Expert Explanation: This clinical presentation is characteristic of systemic anaphylaxis,
which is a Type I hypersensitivity reaction. The allergen cross-links IgE antibodies already
bound to Fc receptors on the surface of mast cells. This triggers the rapid release of pre-
formed mediators like histamine and leukotrienes. These mediators cause smooth muscle
contraction, vasodilation, and increased vascular permeability leading to the symptoms
described. Immediate treatment with epinephrine is required to reverse these life-
threatening systemic effects.
2. Which of the following describes the mechanism of Type II hypersensitivity as seen in
Hemolytic Disease of the Newborn?
A. Antibodies react with antigens on the surface of cells, leading to complement-mediated
lysis
B. IgE antibodies cause the release of vasoactive amines
C. Antigens are recognized by Th1 cells leading to macrophage activation
D. Large immune complexes circulate and deposit in the basement membrane
Correct Answer: A
Expert Explanation: Type II hypersensitivity involves antibody-mediated destruction of
cells by IgG or IgM. In the case of Hemolytic Disease of the Newborn, maternal IgG
antibodies cross the placenta and target fetal Rh+ red blood cells. The binding of these
antibodies activates the classical complement pathway or promotes opsonization and
phagocytosis. This results in the premature destruction of fetal erythrocytes, leading to
severe anemia. It is a tissue-specific reaction rather than a systemic immune complex
disease.
,3. A patient with Systemic Lupus Erythematosus (SLE) experiences kidney damage due to
glomerulonephritis. What is the underlying immunological cause of this organ damage?
A. Sensitized T-cells directly attacking renal tubular cells
B. Direct binding of IgE to the renal endothelium
C. Deposition of soluble antigen-antibody complexes in the glomerular basement
membrane
D. Loss of regulatory T cells leading to spontaneous renal cell apoptosis
Correct Answer: C
Expert Explanation: SLE is a classic example of Type III hypersensitivity, where immune
complexes are formed in the circulation. These complexes are not efficiently cleared and
instead deposit in various tissues, including the kidneys. Once deposited, they activate the
complement system, which recruits neutrophils to the site. The neutrophils release
lysosomal enzymes and reactive oxygen species that cause significant tissue damage. This
process explains why SLE manifests with multi-organ involvement rather than localized
symptoms.
4. In a Tuberculin (PPD) skin test, the redness and induration observed 48 hours after
injection are caused by:
A. Rapid histamine release from local mast cells
B. Accumulation of macrophages and T-cells at the site of injection
C. Neutrophil infiltration due to immune complex deposition
D. Binding of IgM to the injected bacterial proteins
Correct Answer: B
Expert Explanation: The PPD test is a classic example of Type IV or delayed-type
hypersensitivity (DTH). Unlike other types, this reaction is cell-mediated and does not
involve antibodies. When the antigen is injected, memory Th1 cells recognize it and secrete
cytokines like IFN-gamma. These cytokines recruit and activate macrophages, which cause
the characteristic firm swelling and inflammation. The 48-to-72-hour delay reflects the
time required for T-cell migration and cytokine production.
5. Which of the following autoimmune diseases is characterized by antibodies that act as
agonists to a hormone receptor, leading to overproduction of thyroid hormones?
A. Hashimoto’s Thyroiditis
B. Graves’ Disease
C. Myasthenia Gravis
D. Type 1 Diabetes Mellitus
, Correct Answer: B
Expert Explanation: Graves’ disease is a unique autoimmune condition where the body
produces thyroid-stimulating immunoglobulins (TSI). These antibodies bind to the TSH
receptor on thyroid follicular cells and mimic the action of TSH. This continuous
stimulation leads to hyperthyroidism and thyroid gland enlargement. Unlike many
autoimmune diseases that cause tissue destruction, Graves’ disease is characterized by
hyper-function. This makes it an example of a Type II hypersensitivity reaction where the
antibody alters cell signaling.
6. Myasthenia Gravis involves an autoimmune attack on the neuromuscular junction. What is
the specific target of the autoantibodies in this disease?
A. Voltage-gated calcium channels
B. Myelin basic protein
C. Acetylcholine receptors (AChR)
D. Dopamine receptors
Correct Answer: C
Expert Explanation: In Myasthenia Gravis, the immune system produces autoantibodies
against the nicotinic acetylcholine receptors at the postsynaptic membrane. These
antibodies block the binding of acetylcholine and trigger the internalization and
degradation of the receptors. Additionally, complement activation leads to damage of the
postsynaptic folds. This results in impaired neuromuscular transmission, manifesting as
muscle weakness and fatigue. Treatment often includes acetylcholinesterase inhibitors to
increase the concentration of acetylcholine in the synaptic cleft.
7. A 10-month-old male infant presents with recurrent bacterial pneumonia and ear
infections. Lab results show near-zero levels of B cells and all classes of immunoglobulins.
What is the most likely diagnosis?
A. DiGeorge Syndrome
B. Severe Combined Immunodeficiency (SCID)
C. X-linked Agammaglobulinemia (XLA)
D. Common Variable Immunodeficiency (CVID)
Correct Answer: C
Expert Explanation: X-linked Agammaglobulinemia, or Bruton’s disease, is caused by a
mutation in the BTK gene. This mutation prevents the maturation of pre-B cells into mature
B cells in the bone marrow. Consequently, patients lack mature B cells and cannot produce
antibodies, leading to susceptibility to encapsulated bacteria. Because it is X-linked, it
primarily affects males, and symptoms typically appear after maternal antibodies wane.
Therapy usually involves lifelong intravenous immunoglobulin (IVIG) replacements.
University of Central Florida Updated and Latest
Questions and Correct Answers with Rationale
1. A 25-year-old patient presents with sudden onset of wheezing, hives, and hypotension
after a bee sting. Which immunological mechanism is primarily responsible for this
immediate reaction?
A. IgG-mediated cytotoxic cell lysis
B. T-cell mediated delayed hypersensitivity
C. Immune complex deposition in small vessels
D. IgE-mediated mast cell degranulation
Correct Answer: D
Expert Explanation: This clinical presentation is characteristic of systemic anaphylaxis,
which is a Type I hypersensitivity reaction. The allergen cross-links IgE antibodies already
bound to Fc receptors on the surface of mast cells. This triggers the rapid release of pre-
formed mediators like histamine and leukotrienes. These mediators cause smooth muscle
contraction, vasodilation, and increased vascular permeability leading to the symptoms
described. Immediate treatment with epinephrine is required to reverse these life-
threatening systemic effects.
2. Which of the following describes the mechanism of Type II hypersensitivity as seen in
Hemolytic Disease of the Newborn?
A. Antibodies react with antigens on the surface of cells, leading to complement-mediated
lysis
B. IgE antibodies cause the release of vasoactive amines
C. Antigens are recognized by Th1 cells leading to macrophage activation
D. Large immune complexes circulate and deposit in the basement membrane
Correct Answer: A
Expert Explanation: Type II hypersensitivity involves antibody-mediated destruction of
cells by IgG or IgM. In the case of Hemolytic Disease of the Newborn, maternal IgG
antibodies cross the placenta and target fetal Rh+ red blood cells. The binding of these
antibodies activates the classical complement pathway or promotes opsonization and
phagocytosis. This results in the premature destruction of fetal erythrocytes, leading to
severe anemia. It is a tissue-specific reaction rather than a systemic immune complex
disease.
,3. A patient with Systemic Lupus Erythematosus (SLE) experiences kidney damage due to
glomerulonephritis. What is the underlying immunological cause of this organ damage?
A. Sensitized T-cells directly attacking renal tubular cells
B. Direct binding of IgE to the renal endothelium
C. Deposition of soluble antigen-antibody complexes in the glomerular basement
membrane
D. Loss of regulatory T cells leading to spontaneous renal cell apoptosis
Correct Answer: C
Expert Explanation: SLE is a classic example of Type III hypersensitivity, where immune
complexes are formed in the circulation. These complexes are not efficiently cleared and
instead deposit in various tissues, including the kidneys. Once deposited, they activate the
complement system, which recruits neutrophils to the site. The neutrophils release
lysosomal enzymes and reactive oxygen species that cause significant tissue damage. This
process explains why SLE manifests with multi-organ involvement rather than localized
symptoms.
4. In a Tuberculin (PPD) skin test, the redness and induration observed 48 hours after
injection are caused by:
A. Rapid histamine release from local mast cells
B. Accumulation of macrophages and T-cells at the site of injection
C. Neutrophil infiltration due to immune complex deposition
D. Binding of IgM to the injected bacterial proteins
Correct Answer: B
Expert Explanation: The PPD test is a classic example of Type IV or delayed-type
hypersensitivity (DTH). Unlike other types, this reaction is cell-mediated and does not
involve antibodies. When the antigen is injected, memory Th1 cells recognize it and secrete
cytokines like IFN-gamma. These cytokines recruit and activate macrophages, which cause
the characteristic firm swelling and inflammation. The 48-to-72-hour delay reflects the
time required for T-cell migration and cytokine production.
5. Which of the following autoimmune diseases is characterized by antibodies that act as
agonists to a hormone receptor, leading to overproduction of thyroid hormones?
A. Hashimoto’s Thyroiditis
B. Graves’ Disease
C. Myasthenia Gravis
D. Type 1 Diabetes Mellitus
, Correct Answer: B
Expert Explanation: Graves’ disease is a unique autoimmune condition where the body
produces thyroid-stimulating immunoglobulins (TSI). These antibodies bind to the TSH
receptor on thyroid follicular cells and mimic the action of TSH. This continuous
stimulation leads to hyperthyroidism and thyroid gland enlargement. Unlike many
autoimmune diseases that cause tissue destruction, Graves’ disease is characterized by
hyper-function. This makes it an example of a Type II hypersensitivity reaction where the
antibody alters cell signaling.
6. Myasthenia Gravis involves an autoimmune attack on the neuromuscular junction. What is
the specific target of the autoantibodies in this disease?
A. Voltage-gated calcium channels
B. Myelin basic protein
C. Acetylcholine receptors (AChR)
D. Dopamine receptors
Correct Answer: C
Expert Explanation: In Myasthenia Gravis, the immune system produces autoantibodies
against the nicotinic acetylcholine receptors at the postsynaptic membrane. These
antibodies block the binding of acetylcholine and trigger the internalization and
degradation of the receptors. Additionally, complement activation leads to damage of the
postsynaptic folds. This results in impaired neuromuscular transmission, manifesting as
muscle weakness and fatigue. Treatment often includes acetylcholinesterase inhibitors to
increase the concentration of acetylcholine in the synaptic cleft.
7. A 10-month-old male infant presents with recurrent bacterial pneumonia and ear
infections. Lab results show near-zero levels of B cells and all classes of immunoglobulins.
What is the most likely diagnosis?
A. DiGeorge Syndrome
B. Severe Combined Immunodeficiency (SCID)
C. X-linked Agammaglobulinemia (XLA)
D. Common Variable Immunodeficiency (CVID)
Correct Answer: C
Expert Explanation: X-linked Agammaglobulinemia, or Bruton’s disease, is caused by a
mutation in the BTK gene. This mutation prevents the maturation of pre-B cells into mature
B cells in the bone marrow. Consequently, patients lack mature B cells and cannot produce
antibodies, leading to susceptibility to encapsulated bacteria. Because it is X-linked, it
primarily affects males, and symptoms typically appear after maternal antibodies wane.
Therapy usually involves lifelong intravenous immunoglobulin (IVIG) replacements.
