LTHOUGH THE ETIOLOGY and A pathogenesis of rheumatoid arthritis remain obscure, immunologic processes have been thought to play a role in the course of the disease. The earliest immunofluorescent studies of rheumatoid arthritis synovium by Kaplan and Vaughan1P2 and Rodman et aL3 revealed the presence of yG globulin and rheumatoid factor; the latter authors have also showed that PIC and PIE globulin components of complement are deposited within rheumatoid arthritis synovium. Using similar methods, Vazquez and Dixon4 showed that rheumatoid nodules contained large deposits of yG globulin, and Mellors et al. 5 demonstrated production of rheumatoid factors by plasma cells in the synovial tissues. Hollander and coworkers6 and Delbarre7 have recently found that polymorphonuclear leukocytes isolated from the synovial fluid of patients with rheumatoid arthritis contain large cytoplasmic vacuolar inclusions of yG and yM globulins. These findings have been confirmed in part by Riddle et a1.* who demonstrated that fibrin was also present in the leukocyte inclusions. These workers also presented electron microscopic evidence that the vacuoles contained a homogeneous electron-dense material. The present study9 was stimulated by the recent findings of Hedberg et al. lOJ1 and of Pekin and ZvaiflerI2 that the whole complement in the synovial fluid in rheumatoid arthritis is markedly depressed in patients with active disease. Austen et all3 have shown a similar depression in C'2 component of complement. In spite of these changes in the synovial fluid, serum complement levels in rheumatoid arthritis patients are normal or elevated. The purpose of this investigation was to explore the possibility that low joint fluid complement titers may reflect local utilization of complement in an antigen-antibody reaction. The synovial tissues of 15 pa-tients with rheumatoid arthritis were examined by immunohistochemical methods