To identify cytokines responsible for the increased levels of tumor necrosis factor receptor (TNFR) in the joints of patients with rheumatoid arthritis.
Antibodies to TNFR types were used both to inhibit ligand cell binding and to quantify released receptors in rheumatoid synovial fibroblasts.
Binding by and shedding of the p75 TNFR was affected by interleukin-1 (IL-1), IL-4, and interferon-gamma.
IL-1 could cause increased TNF alpha binding and TNFR shedding in inflamed joints.