作者: Johannes A Bezuidenhout , Etheresia Pretorius , None
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摘要: Rheumatoid arthritis (RA) is an autoimmune disease of complex etiopathogenic origin and traditionally characterized by chronic synovitis articular erosions. Furthermore, there strong evidence that infectious agents, including those become dormant within the host, play a major role in much etiology RA its hallmark inflammation. A combination genetic predisposition, environmental exposure, presence agents may therefore lead to loss immune tolerance citrullinated proteins, which present as self-antigens human system. This results generation highly RA-specific autoantibodies, known anti-citrullinated protein antibodies (ACPAs). Protein citrullination occurs via posttranslational deamination arginine residues peptidylarginine deiminase enzymes, have confirmed sources both endogenous origins. recognized plasma target autoantibody fibrin soluble precursor fibrinogen, key components hemostasis acute phase reaction. Increased titers ACPAs accompany rapid progression clinical been shown drive variety proinflammatory processes, aberrant clot formation increased cardiovascular risk. However, full extent affected remains controversial, owing differential impact fibrin(ogen) concurrent systemic inflammation on resulting hemostatic outcome. review highlights events initiation autoimmune-driven inflammatory events, bacterial subsequently result associated secondary risk, with specific focus proteins are heavily involved throughout immunopathological process.