Modulation of helper T cell function by prostaglandins

Kenneth N. Gold, Cornelia M. Weyand, JöRg J. Goronzy

Research output: Contribution to journalArticlepeer-review

84 Scopus citations

Abstract

Objective. To determine the influence of prostaglandins on the production of interleukins 2, 4, and 5 (IL‐2, IL‐4, and IL‐5), interferon‐γ (IFNγ), granulocytemacrophage colony‐stimulating factor, and transforming growth factor β1 by CD4+ T cells. Methods. TH0, TH1, and TH2 T cell clones were stimulated in the presence and absence of the prostaglandin E1 (PGE1) analog misoprostol and PGE2. Lymphokine production was analyzed by using a semiquantitative polymerase chain reaction with lymphokine‐specific primer sets and/or by determining lymphokine activity in bioassays. Results. PGE2 and misoprostol have distinct effects on different functional T helper cells. TH1 cells, which predominantly produce IL‐2 and IFNγ, are completely inhibited, while TH2 cells, which preferentially produce IL‐4 and IL‐5, are largely unaffected. Misoprostol and PGE2 are equivalent in their ability to modulate T cell function. In the presence of prostaglandins, THO‐like helper cells, which are characterized by the coproduction of multiple lymphokines, function as TH2 cells; however, they do not differentiate into TH2 T cells. Conclusion. Prostaglandins that are produced in inflamed tissue can regulate the functional capabilities of infiltrating T cells. In the presence of PGE2, TH1‐like responses are suppressed and TH0‐like responses are shifted toward a TH2‐like pattern dominated by the production of IL‐4 and IL‐5. Inhibition of prostaglandin production by antiinflammatory agents might restore TH1 responses with local production of IL‐2 and IFNγ.

Original languageEnglish (US)
Pages (from-to)925-933
Number of pages9
JournalArthritis & Rheumatism
Volume37
Issue number6
DOIs
StatePublished - Jun 1994

ASJC Scopus subject areas

  • Immunology and Allergy
  • Rheumatology
  • Immunology
  • Pharmacology (medical)

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