Open AccessChloroquine inhibits T cell proliferation by interfering with IL‐2 production and responsiveness
Author(s) -
LANDEWE R. B. M.,
MILTENBURG A. M. M.,
VERDONK M. J. A.,
VERWEIJ C. L.,
BREEDVELD F. C.,
DAHA M. R.,
DIJKMANS B. A. C.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb06648.x
Subject(s) - chloroquine , immunology , cell growth , biology , medicine , microbiology and biotechnology , malaria , genetics
SUMMARY 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.