A Critique of Some of the Current Concepts on the Immunopathogenesis of Rheumatoid Arthritis
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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.