Evidence of an activated T-cell system with augmented turnover of interleukin 2 in rheumatoid arthritis. Stimulation of human T lymphocytes by dendritic cells as a model for rheumatoid T-cell activation.

The stage of activation of synovial inflammatory T cells was studied in rheumatoid arthritis and compared with that of normal T cells stimulated in vitro by dendritic cells. Increased numbers of rheumatoid inflammatory T cells expressed activation antigens such as HLA-DR, interleukin 2 receptors (Tac), and transferrin receptors. These T cells also had high spontaneous proliferation. Peripheral blood T cells stimulated by autologous dendritic cells showed a similar expression of activation antigens and had high proliferation. Resting T cells and T cells cocultured with monocytes expressed much less activation markers. Exogenous interleukin 2 significantly increased the proliferation of the various T cells. All responses were inhibited by an antibody which blocks the interleukin 2 receptor. Supernatants from mitogen-stimulated rheumatoid inflammatory mononuclear cells and mitogen-stimulated T cells preactivated by dendritic cells usually contained less interleukin 2 than supernatants from mitogen-stimulated normal T cells. Furthermore, the various in vivo and in vitro-activated Tac-positive T cells, in contrast to nonactivated Tac-negative T cells from peripheral blood of patients and controls, significantly absorbed interleukin 2. The results indicate a turnover of interleukin 2 in rheumatoid inflammatory T cells comparable to that of T cells activated by dendritic cells.