       Document 0596
 DOCN  M9640596
 TI    Tenidap, but not nonsteroidal anti-inflammatory drugs, inhibits T-cell
       proliferation and cytokine induction.
 DT    9604
 AU    Dolhain RJ; de Kuiper P; Verweij CL; Penders JM; Breedveld FC; Dijkmans
       BA; Miltenburg AM; Department of Rheumatology, University Hospital
       Leiden, The; Netherlands.
 SO    Scand J Immunol. 1995 Dec;42(6):686-93. Unique Identifier : AIDSLINE
       MED/96150319
 AB    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.
 DE    Anti-Inflammatory Agents, Non-Steroidal/*PHARMACOLOGY  Antigens,
       CD3/IMMUNOLOGY  Arthritis, Rheumatoid/DRUG THERAPY/*IMMUNOLOGY  Base
       Sequence  Cell Division/DRUG EFFECTS  Clone Cells
       Cytokines/*BIOSYNTHESIS  DNA Primers  Human  Indoles/*PHARMACOLOGY
       Interleukin-2/IMMUNOLOGY  Lymphocyte Transformation  Molecular Sequence
       Data  RNA, Messenger/METABOLISM  Th1 Cells/*DRUG EFFECTS/IMMUNOLOGY
       JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

