Thyroid stimulating hormone (TSH) Receptor on thyroid cells Thyroxine Gravis Disease Adnylate cyclase Triiodothyronine Autoantibodies to receptor on Thyroid cell Long -acting thyroid stimulation hormones Overstimulation of thyroid utoantibodies against acetyl-choline A receptor on muscle cell in neuromuscular junction Autoantibodies block binding of acetyl-choline Myasthenia gravis Organ Specific utoantibodies internalize and degrade acetylA choline receptor o signal transmission across neuromuscular N junction estrucion of insulin-produceing beta cells in D pancrease. Variation in MHC genes (MHC Class II) Affect ability recognize self/non-self utoantigens: Insulin & Glutamic Acid A decarboxylase (GAD) Type I Diabetes PCs process and present autoantigens to A CD4+ T cells h1, Th17, activated released proT inflammatory cytokines IL1, IFN-gamma, TNF-alpha Destruction of pancreatic beta cell ctivate CD8+ T cells & Natural Killer (NK) A cells kill beta cells Insulin production decrease, leads to hyperglycemia Autoimmune Disease Inflammatory disease of CNS Immune mediated demyelination, neurodegradation Multiple Sclerosis utoreactive T cells recognize myelin protein A as autoantigens ctivated T cell release pro-inflammatory A cytokines IL-1. IFN-gamma, TNF-alpha Inflammation and leads to demyelination Disrupt transmission of nerve signals Mainly affect women any different autoantibodies are found in M patients Non-Organ Specific Systemic Lupus Erythemotosus cells produce autoantibodies against selfB antigens such as DNA, histones, and nuclear components ormation of immune complexes composed of F autoantibodies and specific antigens eposit of the complexes in the blood vessels D in various tissues Immune complex leads to inflammation elease inflammatory cytokines cause R widespread inflammation eficiency of complement proteins C1, C2,C4 D increased incidence of SLE Inflammatory to joints, blood vessels, lungs, tissues Rheumatoid Arthritis D4+ T cells, activated B cells, plasma cell C found in inflamed joint ro-inflammatory cytokines IL-1, TNF in P synovial fluid hickennd synovia membrane, cartilage T degradation, bone erosion