Difference between revisions of "Rheumatoid Arthritis"
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m (Text replace - "Type IV Hypersensitivity - WikiBlood" to "Type IV Hypersensitivity") |
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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. | * 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. | ||
| − | [[Category:Cell Mediated Autoimmune Diseases]][[Category:To Do - | + | [[Category:Cell Mediated Autoimmune Diseases]][[Category:To Do - Clinical]][[Category:To Do - Blood]] |
Revision as of 19:09, 28 November 2010
Pathogenesis:
- Type IV hypersensitivity: CD4 Th-1 cell mediated.
- 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.