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Research Article Free access | 10.1172/JCI114035

Prostaglandin E2 selectively increases interferon gamma receptor expression on human CD8+ lymphocytes.

M N elMasry and R R Rich

Howard Hughes Medical Institute Laboratory, Baylor College of Medicine, Houston, Texas 77030.

Find articles by elMasry, M. in: PubMed | Google Scholar

Howard Hughes Medical Institute Laboratory, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Rich, R. in: PubMed | Google Scholar

Published April 1, 1989 - More info

Published in Volume 83, Issue 4 on April 1, 1989
J Clin Invest. 1989;83(4):1436–1440. https://doi.org/10.1172/JCI114035.
© 1989 The American Society for Clinical Investigation
Published April 1, 1989 - Version history
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Abstract

We previously reported that prostaglandin E2 (PGE2) at a physiologic concentration (10(-8) M) and interferon gamma (IFN gamma), acting sequentially, were required for the differentiation of suppressor cells in mitogen-stimulated cultures. The present study was designed to test whether PGE2 might mediate IFN gamma-dependent effects on CD8+ cells by altering the number and/or affinity of their IFN gamma receptors. CD8+ and CD4+ cells when cultured for 18 h expressed comparable numbers of IFN gamma receptors of a single high affinity. Incubation with 10(-8) M PGE2 for 18 h, however, increased the number of IFN gamma receptors on CD8+ cells without affecting the binding affinity. Similar effects were not observed with CD4+ cells, nor when CD8+ cells were cultured in 10(-8) M PGD2. Concentrations of PGE2, which were ineffective in the induction of IFN gamma-dependent suppressor cell differentiation, also did not affect IFN gamma receptor expression on CD8+ cells. This observation of a specific stimulatory effect of PGE2 on the display of IFN gamma receptors of CD8+ cells suggests a novel mechanism for eicosanoid function through tissue-specific regulation of hormone receptors.

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