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.
|
Authors | S C Gilman, H G Bluestein |
Journal | Agents and actions
(Agents Actions)
Vol. 21
Issue 3-4
Pg. 266-8
(Aug 1987)
ISSN: 0065-4299 [Print] Switzerland |
PMID | 2825478
(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)
|