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| + | {{frontpage |
| + | |pagetitle =Autoimmune Diseases |
| + | |pagebody = |
| + | |contenttitle =Content |
| + | |contentbody =<big><b> |
| + | <categorytree mode=pages>Autoimmune Diseases</categorytree> |
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− | ==[[Antibody Mediated Autoimmune Diseases]]== | + | </b></big> |
| + | |logo =path-logo.png |
| + | }} |
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− | ==Cell mediated autoimmune diseases==
| + | [[Category:Immunological Disorders]] |
− | [[Image:Rheumatoid Arthritis Type IV hypersensitivity.jpg|right|thumb|150px|Rheumatoid Arthritis-Brian Catchpole RVC 2008]]
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− | [[Image:Diabetes Mellitus Type IV hypersensitivity.jpg|right|thumb|150px|Diabetes Mellitus-Brian Catchpole RVC 2008]]
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− | ===1. Rheumatoid arthritis===
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− | '''Pathogenesis:'''
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− | * [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]: CD4 Th-1 cell mediated.
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− | * Macrophages phagocytose self antigens and can present peptides on their MHC Class II molecules. The autoreactive TH-1 cells release IFN-gamma which activates macrophages to release prostaglandins, MMP enzymes and TNF-alpha (pro-inflammatory mediator), see diagram. These cytokines cause inflammation and tissue destruction.
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− | ===2. Diabetes Mellitus type I===
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− | '''Pathogenesis:'''
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− | * [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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− | * The CTLs think that all the beta cells in the pancreas are infected by a virus, as it wrongly detects a self antigen presented by the MHC class I on the surface of the cell as foreign.
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− | * Autoreactive CD8+ CTLs are inadvertently activated, destroying the beta cells, thus preventing the secretion of insulin and causing diabetes type 1 (see diagram).
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− | ===3. Hypothyroidism (lymphocytic throiditis)===
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− | '''Pathogenesis:''' [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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− | * T cell mediated
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− | ===4. Hypoadrenocorticism (Addisons disease)===
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− | '''Pathogenesis:''' [[Type IV Hypersensitivity - WikiBlood|Type IV hypersensitivity]]
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− | [[Category:Lymphoreticular and Haemopoietic Diseases]]
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− | [[Category:Immunology]] | |