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The Journal of Immunology, Vol 155, Issue 10 4604-4612, Copyright © 1995 by American Association of Immunologists
ARTICLES |
K Katamura, N Shintaku, Y Yamauchi, T Fukui, Y Ohshima, M Mayumi and K Furusho
Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
We investigated the effect of prostaglandin E2 on the acquisition of cytokine-producing ability by naive CD4+ T cells in human cord blood. Naive CD4+ T cells were stimulated for 3 days with mouse monoclonal anti-CD3 Ab, then washed and expanded in IL-2-containing medium for 3 more days. These activated T cells produced IL-2, IL-4, IL-5, and IFN- gamma upon stimulation with PMA and ionomycin. PGE2 added at priming of naive T cells inhibited the production of IL-2 and IFN-gamma, but not of IL-4 and IL-5, in a dose-dependent manner. This change in the cytokine production profile induced by PGE2 was maintained in T cells restimulated with anti-CD3 in the absence of PGE2, expanded by IL-2, and stimulated with PMA and ionomycin. The mRNA expression of IFN-gamma and IL-2, but not that of IL-4, was also decreased in these cells. Forskolin and dibutyryl cAMP had a similar effect. PGE2 must exist at an early stage of T cell activation to inhibit priming for IL-2 and IFN- gamma production. PGE2 also showed this effect, even in the presence of exogenous IFN-gamma, at the primary stimulation. These results indicate that PGE2 inhibits the acquisition of the ability to produce IL-2 and IFN-gamma by acting directly on naive T cells. Our results suggest that PGE2 plays a role in facilitating the development of the Th2-type cytokine production profile.
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