In:
Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 102, No. 1 ( 2008-06-28), p. 144-151
Abstract:
Chloroquine (Chi) is an anti-rheumatic drug that is widely used in the treatment of rheumatoid arthritis (RA). It seems that T ceils are important in the pathogenesis of RA, but it is not known whether Chl acts via inhibition of T cell function. We here present evidence that Chl, just like cyclosporine A (CsA), inhibits Tcell proliferation as induced with immobilized αCD3 MoAb in a concentration-dependent manner, at least partly through interfering with the production of IL-2 protein and the induction of IL-2 inRNA. Furthermore, Chi impedes the responsiveness of T cell clones to IL-2 since (1) the inhibition of αCD3 MoAb-induced proliferation by Chi could not be reversed by rlL-2 and (2) Chi directly blocks IL-2-driven proliferation of cloned T cells. Chi appeared to interfere with the internalization (50% inhibition) and degradation (total blockade) of rIL-2. Finally, the combination of Chi and CsA synergistically inhibited T ceil proliferation. We conclude that Chi may inhibit functional properties of human T cells. although the drug is 100-to 1000-folds less potent than CsA in inhibiting T cell proliferation and IL-2 production, respectively. It is speculated that the in vitro. effects of Chl might be relevant in explaining the anti-rheumatic effect of this drug in patients with RA.
Type of Medium:
Online Resource
ISSN:
1365-2249
,
0009-9104
DOI:
10.1111/j.1365-2249.1995.tb06648.x
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
2008
detail.hit.zdb_id:
2020024-9
