Open AccessModulation of helper T cell function by prostaglandins
Author(s) -
Gold Kenneth N.,
Weyand Cornelia M.,
Goronzy JöRg J.
Publication year - 1994
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780370623
Subject(s) - lymphokine , t cell , t helper cell , prostaglandin e , interleukin 4 , prostaglandin e2 , biology , cytokine , immunology , microbiology and biotechnology , chemistry , endocrinology , immune system
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 E 1 (PGE 1 ) analog misoprostol and PGE 2 . 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. PGE 2 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 PGE 2 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 PGE 2 , 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.