Which of the following best defines immunological tolerance?
A. The ability to respond to all antigens equally
B. The immune system’s failure to recognize foreign antigens
C. The immune system’s ability to recognize self-antigens without attacking them
D. The destruction of foreign pathogens by antibodies

C. The immune system’s ability to recognize self-antigens without attacking them

Which factor is most likely to promote tolerance?
A. Low antigen dose
B. Oral or intravenous exposure
C. Strong inflammatory response
D. Presence of co-stimulation

B. Oral or intravenous exposure

Which four factors influence immunological tolerance?
A. Age, sex, MHC type, diet
B. Antigen dose, route, age, co-stimulation
C. Cytokine type, complement, diet, infection
D. T cell type, B cell count, MHC class, age

B. Antigen dose, route, age, co-stimulation

How does tolerance work?
A. By killing all T cells
B. Through deletion, inactivation, or suppression of self-reactive lymphocytes
C. By increasing inflammatory cytokines
D. Through activation of complement

B. Through deletion, inactivation, or suppression of self-reactive lymphocytes

Where does central tolerance occur?
A. Spleen and lymph nodes
B. Bone marrow and thymus
C. Liver and pancreas
D. Peyer’s patches

B. Bone marrow and thymus

Which mechanisms are considered central tolerance?
A. Clonal helplessness, AICD, anergy
B. Clonal deletion, receptor editing, Treg production
C. AICD, Treg suppression, clonal deviation
D. Peripheral anergy, apoptosis, cytokine suppression

B. Clonal deletion, receptor editing, Treg production

What is the function of AIRE in central tolerance?
A. Promotes receptor editing in B cells
B. Controls expression of peripheral antigens in thymus
C. Enhances antibody class switching
D. Activates Tregs in the periphery

B. Controls expression of peripheral antigens in thymus

A mutation in the AIRE gene results in:
A. IPEX
B. APS-1/APECED
C. Multiple sclerosis
D. Rheumatoid arthritis

B. APS-1/APECED

Which of the following is a hallmark of APS-1?
A. Anemia and arthritis
B. Hypoparathyroidism, adrenal failure, and candidiasis
C. Muscle weakness and rash
D. Enlarged lymph nodes

B. Hypoparathyroidism, adrenal failure, and candidiasis

What happens during peripheral anergy?
A. Self-reactive cells are deleted
B. Lymphocytes encounter antigen without co-stimulation and become inactive
C. T cells undergo receptor editing
D. B cells are activated to produce antibodies

B. Lymphocytes encounter antigen without co-stimulation and become inactive

What is clonal helplessness?
A. When T cells fail to receive B cell help
B. When B cells fail to receive T cell help, leading to anergy
C. When both B and T cells are deleted
D. When Tregs suppress inflammation

B. When B cells fail to receive T cell help, leading to anergy

What is the main role of Tregs?
A. Promote inflammation
B. Activate macrophages
C. Suppress immune activation
D. Stimulate antibody production

C. Suppress immune activation

Loss of FOXP3 results in which autoimmune disease?
A. APS-1
B. IPEX
C. Lupus
D. Graves disease

B. IPEX

Which cytokines are secreted by Tregs?
A. IL-4, IL-5
B. IL-10, TGF-β
C. IL-1, IL-6
D. IFN-γ, TNF-α

B. IL-10, TGF-β

Which mechanism eliminates overstimulated or autoreactive T cells via Fas–FasL interaction?
A. Peripheral anergy
B. Activation-induced cell death (AICD)
C. Clonal deviation
D. Receptor editing

B. Activation-induced cell death (AICD)

What is clonal deviation?
A. A shift from a harmful to a less harmful immune response
B. Loss of co-stimulation
C. T cell apoptosis
D. Treg expansion failure

A. A shift from a harmful to a less harmful immune response

What is autoimmunity?
A. Immune tolerance to foreign pathogens
B. Immune response against self-antigens
C. Failure to activate lymphocytes
D. Overproduction of complement

B. Immune response against self-antigens

Type II

Antibody-mediated cytotoxicity

Type III

Immune complex-mediated

Type IV

T-cell mediated

Which type of autoimmunity involves immune complex deposition?
A. Type I
B. Type II
C. Type III
D. Type IV

C. Type III

Which HLA-related factor increases autoimmune susceptibility?
A. Cytokine deficiency
B. MHC presentation of self-peptides
C. Lack of antibodies
D. Elevated TGF-β

B. MHC presentation of self-peptides

What is the function of a GWAS in autoimmunity?
A. Detect infections
B. Identify genetic variants linked to disease
C. Measure cytokine levels
D. Detect antibodies

B. Identify genetic variants linked to disease

What is linkage disequilibrium?
A. Random inheritance of alleles
B. Inheritance of alleles together more often than by chance
C. Mutation in HLA gene
D. Autoimmune deletion

B. Inheritance of alleles together more often than by chance

Why are autoimmune diseases more common in females?
A. Testosterone suppresses immunity
B. Estrogen enhances immune activity
C. Men have stronger tolerance mechanisms
D. Females have fewer Tregs

B. Estrogen enhances immune activity

Which mechanism explains infection-triggered autoimmunity due to antigen similarity?
A. Clonal deletion
B. Molecular mimicry
C. Epitope spreading
D. Peripheral anergy

B. Molecular mimicry

What is bystander activation?
A. Activation of self-reactive lymphocytes by nearby inflammation
B. Suppression of T cell responses
C. Blocking of co-stimulatory signals
D. Cytokine inhibition

A. Activation of self-reactive lymphocytes by nearby inflammation

What is epitope spreading?
A. Broadening of immune response to new self-antigens
B. Mutation of MHC molecules
C. Loss of Treg activity
D. Overactivation of macrophages

A. Broadening of immune response to new self-antigens

Which condition best represents a systemic autoimmune disease?
A. Type 1 diabetes
B. Lupus erythematosus
C. Hashimoto’s thyroiditis
D. Multiple sclerosis

B. Lupus erythematosus

What distinguishes Type II autoimmunity (e.g., Graves) from Type IV (e.g., MS)?
A. Type II is antibody-mediated, Type IV is T-cell mediated
B. Type II is T-cell mediated, Type IV is antibody-mediated
C. Both are immune complex diseases
D. Type IV only affects the skin

A. Type II is antibody-mediated, Type IV is T-cell mediated

What is Tysabri (Natalizumab)?
A. A corticosteroid
B. A monoclonal antibody that blocks α4 integrin to prevent immune cell entry to brain
C. A complement inhibitor
D. A Treg-inducing cytokine

B. A monoclonal antibody that blocks α4 integrin to prevent immune cell entry to brain

What did Tysabri teach us about immune privilege?
A. Blocking immune access can disrupt surveillance, increasing infection risk
B. Immune privilege has no clinical relevance
C. CNS immunity is independent of T cells
D. Autoimmunity only affects peripheral tissues

A. Blocking immune access can disrupt surveillance, increasing infection risk

What is IVIG and how does it help?
A. Pooled IgG that neutralizes autoantibodies and modulates immune responses
B. Synthetic cytokine to boost T cell activity
C. Vaccine to induce tolerance
D. Antibody that destroys Tregs

A. Pooled IgG that neutralizes autoantibodies and modulates immune responses