Immune Lecture 24 Study Notes.docx

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Microbiology and Immunology
Microbiology and Immunology 3300B

Immune Lecture 24 Study Notes 1. What is an autoimmune disease? -broadly classified as “systemic” or “organ-specific” -possible to have more than one disease: depends on the immune mechanism responsible -arthritis, scleroderma and lupus are systemic autoimmune diseases -MS/diabetes are organ specific 2. Which hypersensitivities classify as autoimmune diseases? -2,3 and 4 3. What hypersensitivity does arthritis deal with? -type 3: rheumatoid factor (is an antibody that binds IgG)  becomes an immune complex 4. Discuss the diseases an the types of autoantigens they have. -lupis  many antibodies to antigens (DNA/RNA/histone/proteins) -arthritis  RF to IgG -when the cells get killed: messy cell death; these are available to the body – bind all over the body = huge systemic response 5. What is systemic lupus erythematasos (SLE)? -type 3 hypersensitivity -immune complex-mediated disease that deposit on small blood vessel walls -c’ and FcR mediated tissue destruction -affects the kidneys, skin, muscles, joints, lungs, heart and brain -butterfly rash is common 6. Discuss the tissue-specific hypersensitivity. -type 2 hypersensitivity -IgG against cell surface antigen -cell destruction through compliment or FcR -alters signaling or functioning -receptor blockade or activation -ex/ autoimmune hemolytic anemia 7. What is autoimmune hemolytic anemia? -red blood cells are attached to anti-RBC autoantibodies -FcR cells cause phagocytosis -complement activation and intravascular hemolysis -this results in a short half life = anemia 8. What is autoimmune thrombocytopenic purpura? -type 2 hypersensitivity -platelets are depleted which means you don’t clot well and bruise easily -this also alters signaling through receptors 9. What is Graves’ disease? -type 2 hypersensivity -normally, the pituitary gland will secrete thyroid sitmulating hormone (TSH) which acts on the thyroid to induce the release of thyroid hormones; these will act on the pituitary to shut down production of TSH which suppresses further thyroid hormone synthesis (feedback suppression) -in graves disease: autoimmune B cells make antibodies against TSH receptor that also stimulate thyroid hormone production; thyroid hormones will shut down TSH production but have no effect on the autoantibody production which continues to cause excessive thyroid hormone production -this is an agonist activity 10.What results from hyperthyroidism? -heat, increased appeptite, weight loss, other hormone-related symptoms 11.What is insulin-dependent diabetes mellitus? -type 1 diabetes and is a type 4 hypersensitivity -CD8 T cell-mediated specific destruction of insulin-producing beta islet cells (glucagon and somatostatin are still produced) 12.What is MS? -type 4 hypersensitivity -immune response initiated in second lymphoid tissue -get activated T cells able to access the CNS which induce local inflammation and destruction of myelin 13.What is the mechanism? -there is an unknown trigger that sets up the initial focus of inflammation in the brain and blood brain barrier – becomes locally permeable to leukocytes and blood proteins -T cells specific for CNS antigen and activated peripheral lymphoid tissues reencounter AP of myelin peptides on microglia in the brain -inflammatory reaction in brain due to mast-cell activation, complement activation, antibodies and cytokines -this causes demyelination of neurons TH1 or TH17? 14.What are some common animal models of autoimmune disorders? -NOD (non obese diabetic)  mutation spontaneously occurs – human disease is type 1 diabetes -MRL/lpr  occurs spontaneously; is FAS deficient = autoreactive cells (lupus) -experimental autoimmune encephalitis in SJL (EAE) causes MS – induced with myelin -collagen induced arthritis in DBA/1 causes rheumatoid arthritis – uses collagen as a peptide to induce it -transgenic: bcl-2 transgene causes lupis (its an important regulator of apoptosis – if bcl-2 is protected from apoptosis hen
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