
Effect of rapamycin on the expression of the IL‐2 receptor (CD25)
Author(s) -
WOERLY G.,
BROOKS N.,
RYFFEL B.
Publication year - 1996
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 - 10.1046/j.1365-2249.1996.d01-616.x
Subject(s) - immunology , il 2 receptor , biology , receptor , immune system , t cell , genetics
The immunosuppressive macrolide rapamycin inhibits cytokine‐driven proliferation of lymphocytes, acting at a later stage of T lymphocyte activation than the related compound FK506 or cyclosporin, which block IL‐2 transcription. However, the effect of rapamycin on the expression of the IL‐2 receptor α‐chain (CD25) is less well documented. This study has investigated the effect of rapamycin on mRNA levels of CD25 and membrane expression of IL‐2 receptor in human primary T lymphocytes activated by various stimuli. Rapamycin surprisingly inhibits CD25 upregulation subsequent to anti‐CD3 or ionomycin stimulation. These effects are not secondary to an IL‐2 mediated CD25 up‐regulation, as rapamycin inhibits neither IL‐2 synthesis nor IL‐2‐induced CD25 mRNA. Interestingly, sensitivity to rapamycin correlates with the requirement of de novo protein synthesis, as demonstrated by anisomycin inhibition of both ionomycin‐ and CD3‐induced CD25 transcription. Thus, rapamycin inhibition of T cell activation may involve not only IL‐2 driven proliferation, but also suppression of CD25 up‐regulation.