TENIDAP, BUT NOT NONSTEROIDAL ANTIINFLAMMATORY DRUGS, INHIBITS T-CELLPROLIFERATION AND CYTOKINE INDUCTION

T-lymphocytes are involved in the inflammatory response that occurs in affected joints of patients with rheumatoid arthritis (RA). Some seco nd-line disease modifying anti-rheumatic drugs used in the treatment o f patients with RA are known to block T-cell activation. The present s tudy assessed whether tenidap, an investigational anti-rheumatic drug, affects in vitro T-cell responses such as proliferation and cytokine production. It was found that tenidap, in contrast to several nonstero idal anti-inflammatory drugs, inhibits anti-CD3 or IL-2 driven prolife rative responses of cloned human T-cells. Furthermore, tenidap was fou nd to inhibit IFN-gamma production as well as the induction of mRNA en coding IFN-gamma or TNF-alpha. The results indicate that tenidap may e xert at least part of its anti-inflammatory activity via inhibition of T-cell function and cytokine production.