Abstract
We have previously described a selective defect of monocyte C3b receptor-mediated phagocytosis in patients with rheumatoid cutaneous vasculitis. We have studied a further 15 rheumatoid arthritis patients with other associated diseases and complications and have identified 4 further patients with a similar defect. Serological and cytochemical studies suggest that the defect in phagocytosis is due to the appearance of increased numbers of large nonspecific esterase-negative mononuclear phagocytes with defective C3b receptor phagocytic function rather than to receptor blockade by immune complexes.