Tolerance & Autoimmunity PPT PDF

TOLERANCE & AUTOIMMUNITY – DR. HUSSEIN (6TH PPT) 1. What is immunologic tolerance? A: The acquisition of specific nonresponsiveness to a molecule recognized as nonself by the immune system. 2. What is a tolerogen? A: An immunogenic substance that induces immunologic tolerance rather than immunity...

TOLERANCE & AUTOIMMUNITY – DR. HUSSEIN (6TH PPT) 1. What is immunologic tolerance? A: The acquisition of specific nonresponsiveness to a molecule recognized as nonself by the immune system. 2. What is a tolerogen? A: An immunogenic substance that induces immunologic tolerance rather than immunity due to its chemical composition, dose, or route of introduction. 3. What is anergy? A: The absence of a cell-mediated immune reaction in sensitized individuals, leading to no allergic response to an immunogen or allergen. 4. What is central tolerance? A: The deletion of immature lymphocytes that recognize self-antigens in the thymus or bone marrow. 5. What is peripheral tolerance? A: The inactivation or deletion of mature self-reactive lymphocytes in peripheral tissues after encountering self-antigens. 6. How do naive lymphocytes respond to immunogenic antigens? A: They are activated to proliferate and differentiate. 7. What happens when tolerogenic antigens are encountered by lymphocytes? A: They induce anergy or apoptosis, rendering the lymphocytes unresponsive to the antigen. 8. What factors influence tolerance induction? A: Immunologic maturity, antigen dose, antigen's physicochemical nature, immunogenicity, route of administration, and the type of recipient. 9. What are the three mechanisms of self-tolerance induction? A: Clonal deletion, anergy, and regulated inhibition of antigen-reactive T and B cells. 10. Where does positive and negative selection of T cells occur? A: In the thymus. 11. What is the role of CTLA-4 in T cell tolerance? A: CTLA-4 inhibits T cell activation by binding to B7, blocking further IL-2 synthesis, and leading to cell death. 12. What happens during clonal abortion in B cells? A: High concentrations of multivalent antigens cause immature B cells to abort, preventing further differentiation. 13. What is clonal deletion in B cells? A: The deletion of mature B cells due to strong negative signals, such as the absence of T helper cells. 14. What is clonal anergy in B cells? A: B cells become anergic when exposed to intermediate concentrations of multivalent antigens without further differentiation. 15. How does B cell tolerance differ from T cell tolerance in duration? A: B cell tolerance is shorter because B cells are continually produced, while T cell tolerance lasts longer. 16. What are the advantages of tolerance? A: Self-tolerance, tolerance to foreign grafts, gene therapy, and control of harmful immune responses like hypersensitivity and autoimmune diseases. 17. What are the disadvantages of tolerance? A: Tolerance to certain foreign pathogens and tolerance to self-antigens associated with cancer. 18. What is autoimmunity? A: The immune system's response to self-tissues or antigens, leading to pathological consequences and autoimmune diseases. 19. What genetic factors contribute to autoimmune diseases? A: Genetic predispositions, such as inheritance of certain HLA alleles, play a role in diseases like SLE and Type 1 diabetes. 20. What environmental factors can trigger autoimmune diseases? A: The release of sequestered antigens due to injuries or infections can trigger autoimmunity. 21. What are privileged tissues? A: Tissues like the CNS, brain, eyes, testes, and placenta that are usually sequestered from the immune system. 22. How can the absence of T helper (TH) cells lead to tolerance? A: Without TH cells, B cells do not produce autoantibodies, resulting in tolerance. 23. What happens when suppressor T cells (Ts) are impaired? A: Autoimmune responses may result from the lack of regulatory control by Ts cells. 24. What is the role of MHC II in autoimmune diseases? A: Cells that present MHC II to TH cells can trigger autoimmunity by acting as antigen- presenting cells. 25. How can bacterial and viral infections contribute to autoimmunity? A: Streptococcal infections and EBV can cause polyclonal activation of B cells, leading to autoimmunity. 26. What is molecular mimicry? A: A mechanism where microbial antigens resemble self-antigens, leading to an immune response against self-tissues. 27. What is central T cell tolerance? A: The deletion of T cells that strongly recognize self-antigens during their development in the thymus. 28. What is T cell anergy? A: The functional inactivation of T cells when they recognize antigens without costimulatory signals. 29. What is activation-induced cell death (AICD)? A: The process where repeated antigen exposure leads to Fas-FasL-mediated apoptosis in T cells. 30. What is autoimmune lymphoproliferative syndrome (ALPS)? A: A condition characterized by apoptosis-related autoimmune disease due to mutations in Fas and FasL genes. 31. How do regulatory T cells suppress immune responses? A: By secreting inhibitory cytokines such as IL-10 and TGF-beta or by contact-dependent mechanisms. 32. What features of antigens influence the choice between tolerance and activation in T cells? A: Protein antigens' form, dose, and mode of presentation can determine whether they induce tolerance or activate T cells. 33. What happens to immature B cells that recognize self-antigens? A: They undergo apoptosis or receptor editing to change their specificity. 34. What is peripheral tolerance in B cells? A: The functional inactivation of mature B cells that recognize self-antigens without T cell help. 35. What is the relationship between MHC alleles and autoimmune diseases? A: Inheriting certain MHC alleles increases the risk of developing autoimmune diseases, such as HLA-B27 and ankylosing spondylitis. 36. What is ankylosing spondylitis? A: A chronic inflammatory disease that affects the spine and is associated with the HLA-B27 allele. 37. What is pemphigus? A: An autoimmune disease characterized by blisters on the skin due to autoantibodies attacking skin cells. 38. How do non-MHC genes contribute to autoimmune diseases? A: Genes like Lpr and gld influence immune regulation and contribute to diseases like ALPS. 39. How can microbes promote autoimmunity? A: By activating APCs to present self-antigens with costimulation, or through molecular mimicry. 40. What is autoimmune hemolytic anemia? A: A disease where autoantibodies target red blood cells, leading to their destruction. 41. What is myasthenia gravis? A: An autoimmune disease where autoantibodies block acetylcholine receptors, causing muscle weakness. 42. What is Graves' disease? A: An autoimmune disorder where autoantibodies stimulate the thyroid gland, leading to hyperthyroidism. 43. What is systemic lupus erythematosus (SLE)? A: An immune complex-mediated autoimmune disease characterized by the formation of autoantibodies, especially against DNA. 44. What is multiple sclerosis (MS)? A: A T-cell-mediated autoimmune disease that damages the myelin sheath of nerve cells. 45. What is Type 1 diabetes mellitus? A: A T-cell-mediated autoimmune disease where the immune system attacks insulin-producing beta cells in the pancreas. 46. What is Hashimoto's thyroiditis? A: An autoimmune disease where T cells attack the thyroid, leading to hypothyroidism. 47. What is rheumatoid arthritis? A: A chronic autoimmune disease characterized by inflammation of the joints and the presence of rheumatoid factor. 48. What causes glomerulonephritis? A: Immune complexes deposit in the glomeruli, causing inflammation and kidney damage, often following a streptococcal infection. 49. What is the significance of low complement levels in autoimmune diseases? A: Low complement levels are often seen in active autoimmune diseases like lupus and rheumatoid arthritis, indicating immune complex formation. 50. How are lumpy deposits related to autoimmune diseases? A: Lumpy deposits of immunoglobulins and complement on tissues like the kidneys are markers of immune complex-mediated diseases such as lupus nephritis.