Abstract: The concept that rheumatoid arthritis (RA) is an autoimmune disease is supported by variety of autoantibodies in patient's serum. The most important of these are rheumatoid factors (RFs), antibodies that react with the patient's own Ig. It has been suggested that IgM-RF plays a role in disease pathogenesis. The main source of IgM-RF are B cells that express the pan T-cell marker, CDS: We conducted this study to test the hypothesis that expanded populations of CDS+ B-cells in RA are associated with exacerbation. The RA group consisted of 41 individuals. 20 healthy blood donors were included as normal controls. 17 patients with other collagenous diseases were our patient-control. Cyto-fluorimetric analysis of peripheral blood mononuclear cells was used. The mean % of CD5+ B-cells was significantly greater in patients with RA (without drug) than in healthy controls. The !eve of circulating CD5+B-lymphocytes in RA patients (with drug) was intermediate between that of RA patients (with drug) and healthy controls, showing, that treatment can affect level of CD5+Bcells. There was no significant difference between % of CD5+ B-cells in patients with active and inactive RA. The role of CD5+ B-cells in RA is probably linked to their capacity to produce IgM-RF, which may play a role in pathophysiology of RA. It seems reasonable to postulate that expansion of CD5+ B-cell population, whether due to presence of an Ag such as EBV or other microorganisms, can be responsible for IgM-RF in RA. Whether this expansion represents dysregulatin of a separate cell population normally kept within strict limits, or is a sign of B-cell activation remains unknown.