Print 20 BMD 430 lecture 20 flashcards

20 BMD 430 lecture 20

front 1 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	back 1 C. The immune system’s ability to recognize self-antigens without attacking them
front 2 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	back 2 B. Oral or intravenous exposure
front 3 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	back 3 B. Antigen dose, route, age, co-stimulation
front 4 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	back 4 B. Through deletion, inactivation, or suppression of self-reactive lymphocytes

front 5 Where does central tolerance occur? A. Spleen and lymph nodes B. Bone marrow and thymus C. Liver and pancreas D. Peyer’s patches	back 5 B. Bone marrow and thymus
front 6 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	back 6 B. Clonal deletion, receptor editing, Treg production
front 7 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	back 7 B. Controls expression of peripheral antigens in thymus
front 8 A mutation in the AIRE gene results in: A. IPEX B. APS-1/APECED C. Multiple sclerosis D. Rheumatoid arthritis	back 8 B. APS-1/APECED

front 9 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	back 9 B. Hypoparathyroidism, adrenal failure, and candidiasis
front 10 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	back 10 B. Lymphocytes encounter antigen without co-stimulation and become inactive
front 11 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	back 11 B. When B cells fail to receive T cell help, leading to anergy
front 12 What is the main role of Tregs? A. Promote inflammation B. Activate macrophages C. Suppress immune activation D. Stimulate antibody production	back 12 C. Suppress immune activation

front 13 Loss of FOXP3 results in which autoimmune disease? A. APS-1 B. IPEX C. Lupus D. Graves disease	back 13 B. IPEX
front 14 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	back 14 B. IL-10, TGF-β
front 15 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	back 15 B. Activation-induced cell death (AICD)
front 16 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	back 16 A. A shift from a harmful to a less harmful immune response

front 17 What is autoimmunity? A. Immune tolerance to foreign pathogens B. Immune response against self-antigens C. Failure to activate lymphocytes D. Overproduction of complement	back 17 B. Immune response against self-antigens
front 18 Type II	back 18 Antibody-mediated cytotoxicity
front 19 Type III	back 19 Immune complex-mediated
front 20 Type IV	back 20 T-cell mediated

front 21 Which type of autoimmunity involves immune complex deposition? A. Type I B. Type II C. Type III D. Type IV	back 21 C. Type III
front 22 Which HLA-related factor increases autoimmune susceptibility? A. Cytokine deficiency B. MHC presentation of self-peptides C. Lack of antibodies D. Elevated TGF-β	back 22 B. MHC presentation of self-peptides
front 23 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	back 23 B. Identify genetic variants linked to disease
front 24 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	back 24 B. Inheritance of alleles together more often than by chance

front 25 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	back 25 B. Estrogen enhances immune activity
front 26 Which mechanism explains infection-triggered autoimmunity due to antigen similarity? A. Clonal deletion B. Molecular mimicry C. Epitope spreading D. Peripheral anergy	back 26 B. Molecular mimicry
front 27 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	back 27 A. Activation of self-reactive lymphocytes by nearby inflammation
front 28 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	back 28 A. Broadening of immune response to new self-antigens

front 29 Which condition best represents a systemic autoimmune disease? A. Type 1 diabetes B. Lupus erythematosus C. Hashimoto’s thyroiditis D. Multiple sclerosis	back 29 B. Lupus erythematosus
front 30 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	back 30 A. Type II is antibody-mediated, Type IV is T-cell mediated
front 31 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	back 31 B. A monoclonal antibody that blocks α4 integrin to prevent immune cell entry to brain
front 32 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	back 32 A. Blocking immune access can disrupt surveillance, increasing infection risk

front 33

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

back 33

A. Pooled IgG that neutralizes autoantibodies and modulates immune responses

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20 BMD 430 lecture 20