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Effects of tilomisole, indomethacin and levamisole on regulation of Epstein Barr virus-induced B cell proliferation by peripheral blood mononuclear cells from normal individuals and patients with rheumatoid arthritis.

Abstract
When activated in autologous mixed leukocyte reactions (auto-MLR) in vitro, T cells from normal individuals produce a suppressor factor(s) which inhibits the Epstein-Barr virus (EBV)-induced proliferation of normal B cells. In contrast, T cells from patients with rheumatoid arthritis (RA) are deficient in their ability to generate this suppressor factor in auto-MLR. Addition of tilomisole (Wy-18,251; 33(p-chlorophenyl)thiazolo[3,2-a]benzimidazole-2-acetic acid) to the auto-MLR (0.1-100 micrograms/ml) did not alter the production of suppressor activity by normal T cells, but 100 micrograms/ml tilomisole restored to normal the defective factor production by RA T cells. Indomethacin (1 microgram/ml) but not levamisole (0.1-100 micrograms/ml) had a similar effect, which suggests that the action of tilomisole in this system is due to its ability to inhibit prostaglandin biosynthesis. Nonetheless, the ability of tilomisole to down-regulate B cell function may contribute to the compound's antiarthritic activity.
AuthorsS C Gilman, H G Bluestein
JournalAgents and actions (Agents Actions) Vol. 21 Issue 3-4 Pg. 266-8 (Aug 1987) ISSN: 0065-4299 [Print] Switzerland
PMID2825478 (Publication Type: Journal Article)
Chemical References
  • Benzimidazoles
  • Levamisole
  • tilomisole
  • Indomethacin
Topics
  • Arthritis, Rheumatoid (drug therapy, immunology)
  • B-Lymphocytes (drug effects, immunology)
  • Benzimidazoles (pharmacology)
  • Herpesvirus 4, Human (immunology)
  • Humans
  • In Vitro Techniques
  • Indomethacin (pharmacology)
  • Levamisole (pharmacology)
  • Lymphocyte Activation (drug effects)

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