PCB 3233 Immunology
Exam 4
1. What is the primary immune mechanism responsible for Type I hypersensitivity
reactions?
Answer: Type I hypersensitivity is mediated by IgE antibodies that bind to FcεRI
receptors on mast cells and basophils. Upon allergen exposure, crosslinking of IgE
leads to mast cell degranulation and release of histamine, leukotrienes, and
prostaglandins, causing immediate allergic symptoms.
2. During a Type II hypersensitivity reaction, how are host cells damaged?
Answer: In Type II hypersensitivity, IgG or IgM antibodies target cell surface antigens
on host cells, activating complement or antibody-dependent cellular cytotoxicity
(ADCC), leading to cell lysis or opsonization.
Example: Hemolytic anemia caused by penicillin binding to red blood cells.
3. Which hypersensitivity reaction type involves T-cell mediated tissue damage?
Answer: Type IV hypersensitivity (delayed-type hypersensitivity) involves CD4⁺ Th1
and Th17 cells or CD8⁺ cytotoxic T cells, leading to macrophage activation and tissue
inflammation (e.g., tuberculin skin test or contact dermatitis).
4. Which autoimmune disease is characterized by anti-TSH receptor antibodies that
stimulate thyroid hormone production?
,Answer: Graves’ disease — caused by autoantibodies that mimic TSH, leading to
hyperthyroidism.
5. In systemic lupus erythematosus (SLE), what type of hypersensitivity is primarily
involved?
Answer: Type III hypersensitivity, due to immune complex deposition (DNA–anti-
DNA complexes) that activate complement and cause inflammation in tissues like
kidneys and joints.
6. What is the difference between central and peripheral tolerance?
Answer:
Central tolerance occurs in the thymus (T cells) or bone marrow (B cells) through
deletion or editing of self-reactive lymphocytes.
Peripheral tolerance involves anergy, suppression by Tregs, or immune ignorance to
prevent activation of self-reactive cells that escaped central deletion.
7. Which cytokines are crucial for maintaining regulatory T cell (Treg) function?
Answer: IL-10 and TGF-β — both are immunosuppressive cytokines secreted by Tregs
to inhibit inflammatory T cells and maintain tolerance.
8. What is the main immune mechanism responsible for acute graft rejection?
Answer: Acute rejection is primarily T-cell mediated (Type IV hypersensitivity). CD8⁺
cytotoxic T cells and CD4⁺ Th1 cells recognize alloantigens on the donor tissue and
cause cytotoxicity and inflammation.
, 9. What immunological mechanism is responsible for hyperacute transplant
rejection?
Answer: Pre-existing recipient antibodies (usually IgG) bind to donor endothelial
antigens (ABO or HLA) and activate complement, leading to immediate thrombosis
and necrosis of the graft.
10. What is the primary function of immune checkpoint molecules like PD-1 and
CTLA-4?
Answer: These molecules deliver inhibitory signals to T cells, preventing
overactivation. Tumor cells often exploit PD-1/PD-L1 interactions to evade immune
destruction.
11. How do tumors evade immune surveillance?
Answer: Mechanisms include:
Downregulation of MHC I expression
Secretion of immunosuppressive cytokines (e.g., TGF-β)
Expression of checkpoint ligands (e.g., PD-L1)
Induction of Tregs in the tumor microenvironment.
12. Which type of vaccine uses a live, but weakened, form of the pathogen?
Answer: Live attenuated vaccines, such as MMR or varicella, elicit strong cellular and
humoral immune responses.
13. Why are conjugate vaccines (e.g., Hib) more effective in young children?
Exam 4
1. What is the primary immune mechanism responsible for Type I hypersensitivity
reactions?
Answer: Type I hypersensitivity is mediated by IgE antibodies that bind to FcεRI
receptors on mast cells and basophils. Upon allergen exposure, crosslinking of IgE
leads to mast cell degranulation and release of histamine, leukotrienes, and
prostaglandins, causing immediate allergic symptoms.
2. During a Type II hypersensitivity reaction, how are host cells damaged?
Answer: In Type II hypersensitivity, IgG or IgM antibodies target cell surface antigens
on host cells, activating complement or antibody-dependent cellular cytotoxicity
(ADCC), leading to cell lysis or opsonization.
Example: Hemolytic anemia caused by penicillin binding to red blood cells.
3. Which hypersensitivity reaction type involves T-cell mediated tissue damage?
Answer: Type IV hypersensitivity (delayed-type hypersensitivity) involves CD4⁺ Th1
and Th17 cells or CD8⁺ cytotoxic T cells, leading to macrophage activation and tissue
inflammation (e.g., tuberculin skin test or contact dermatitis).
4. Which autoimmune disease is characterized by anti-TSH receptor antibodies that
stimulate thyroid hormone production?
,Answer: Graves’ disease — caused by autoantibodies that mimic TSH, leading to
hyperthyroidism.
5. In systemic lupus erythematosus (SLE), what type of hypersensitivity is primarily
involved?
Answer: Type III hypersensitivity, due to immune complex deposition (DNA–anti-
DNA complexes) that activate complement and cause inflammation in tissues like
kidneys and joints.
6. What is the difference between central and peripheral tolerance?
Answer:
Central tolerance occurs in the thymus (T cells) or bone marrow (B cells) through
deletion or editing of self-reactive lymphocytes.
Peripheral tolerance involves anergy, suppression by Tregs, or immune ignorance to
prevent activation of self-reactive cells that escaped central deletion.
7. Which cytokines are crucial for maintaining regulatory T cell (Treg) function?
Answer: IL-10 and TGF-β — both are immunosuppressive cytokines secreted by Tregs
to inhibit inflammatory T cells and maintain tolerance.
8. What is the main immune mechanism responsible for acute graft rejection?
Answer: Acute rejection is primarily T-cell mediated (Type IV hypersensitivity). CD8⁺
cytotoxic T cells and CD4⁺ Th1 cells recognize alloantigens on the donor tissue and
cause cytotoxicity and inflammation.
, 9. What immunological mechanism is responsible for hyperacute transplant
rejection?
Answer: Pre-existing recipient antibodies (usually IgG) bind to donor endothelial
antigens (ABO or HLA) and activate complement, leading to immediate thrombosis
and necrosis of the graft.
10. What is the primary function of immune checkpoint molecules like PD-1 and
CTLA-4?
Answer: These molecules deliver inhibitory signals to T cells, preventing
overactivation. Tumor cells often exploit PD-1/PD-L1 interactions to evade immune
destruction.
11. How do tumors evade immune surveillance?
Answer: Mechanisms include:
Downregulation of MHC I expression
Secretion of immunosuppressive cytokines (e.g., TGF-β)
Expression of checkpoint ligands (e.g., PD-L1)
Induction of Tregs in the tumor microenvironment.
12. Which type of vaccine uses a live, but weakened, form of the pathogen?
Answer: Live attenuated vaccines, such as MMR or varicella, elicit strong cellular and
humoral immune responses.
13. Why are conjugate vaccines (e.g., Hib) more effective in young children?
