AbstractIt has been demonstrated that T cells bearing HLA‐DR antigens on their surface are actively involved in an immune response. In diseases of disordered immunoregulation, including rheumatoid arthritis (RA), there are elevated numbers of circulating HLA‐DR + T cells. In this study, we examined the cellular physiology of these T cells in RA patients. Using tritiated thymidine incorporation, we found that, in most patients, HLA‐DR + cells do not account for a significant amount of spontaneous proliferation found in peripheral blood T cells. RNA hybridization studies, using a cloned HLA‐DR alpha chain gene probe, indicate that the T cells actively synthesize HLA‐DR antigens rather than passively adsorbing them. The cell surface phenotype of the HLA‐DR + T cells was analyzed using double immunofluorescence and a variety of monoclonal antibodies. The expression of T cell differentiation antigens T4, T6, T8, and T10 varied markedly from patient to patient. In some patients, a significant number of cells expressed both T4 and T8 antigens. Most HLA‐DR + cells also express antigens defined by the following antibodies: anti‐Tac (the interleukin‐2 receptor), J2 (a glycoprotein found on T cell blasts), and ILR‐1 (a class II major histocompatibility complex antigen). Activated T cells bearing HLA‐DR antigens may play a role in the development of RA. Our data demonstrate that although these cells are not lymphoblasts, they possess a distinct c
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