Activated synovial T cell clones from a patient with rheumatoid arthritis induce proliferation of autologous peripheral blood-derived T cells.

In order to investigate cellular interactions involved in the development of human autoimmune disease, a synovial fluid-derived T cell clone reactive with mycobacterial antigens, termed k38, was employed as a stimulus for autologous peripheral blood mononuclear cells (PBMC). Stimulator cells were used either activated with immobilized OKT3 mAb or in a resting state. Activated k38 cells triggered PBMC to proliferate. A T cell line prepared by coculturing autologous PBMC with irradiated activated k38 cells proliferated upon stimulation with activated k38 cells in the presence of PBMC as a source of accessory cells, as did T cell clones that were subsequently isolated from this line. Blocking studies revealed that proliferation of the anti-k38 line and anti-k38 clones in response to stimulation with clone k38 could be inhibited by monoclonal antibodies against a variety of cellular determinants including HLA class I and LFA-1 beta. It was demonstrated that the antigen reactivity of clone k38 was modulated by the presence of anti-k38 clones. These data provide a model for understanding the cellular interactions that may take place in vivo in the evolution of the chronic synovial inflammatory process.