A critique of some of the current concepts on the immunopathogenesis of rheumatoid arthritis.
The interaction of polycations produced during tissue damage and C-reactive protein, and the enzymatic degradation of complement components may be positive mechanisms augmenting immune-complex/complement damage, while reduced phagocytosis and reduced chemotaxis may be negative mechanisms. In cell-mediated immunity, systems consisting of C-reactive protein, proteases, prostaglandins and immune complexes are all potentially capable of negative feedback control.
D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002634:Chemotaxis, Leukocyte; D003165:Complement System Proteins / Q000378:metabolism; D006801:Humans; D007105:Immune Complex Diseases; D007111:Immunity, Cellular; D010587:Phagocytosis
D003165:Complement System Proteins; D002097:C-Reactive Protein