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Tenidap, but not Nonsteroidal Anti‐Inflammatory Drugs, Inhibits T‐Cell Proliferation and Cytokine Induction

1995; Wiley; Volume: 42; Issue: 6 Linguagem: Inglês

10.1111/j.1365-3083.1995.tb03712.x

1365-3083

Radboud J. E. M. Dolhain, Patricia Kuiper, C. L. Verweij, J. M. A. FENDERS, F C Breedveld, Ben A. C. Dijkmans, A. M. M. Miltenburg,

Cytokine Signaling Pathways and Interactions

T-lymphocytes are involved in the inflammatory response that occurs in affected joints of patients with rheumatoid arthritis (RA). Some second-line disease modifying anti-rheumatic drugs used in the treatment of patients with RA are known to block T-cell activation. The present study 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 nonsteroidal anti-inflammatory drugs, inhibits anti-CD3 or IL-2 driven proliferative responses of cloned human T-cells. Furthermore, tenidap was found to inhibit IFN-gamma production as well as the induction of mRNA encoding IFN-gamma or TNF-alpha. The results indicate that tenidap may exert at least part of its anti-inflammatory activity via inhibition of T-cell function and cytokine production.