MODULATION OF HELPER T-CELL FUNCTION BY PROSTAGLANDINS
MODULATION OF HELPER T-CELL FUNCTION BY PROSTAGLANDINS
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DOI：
10.1002/art.1780370623
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发表时间：
1994-06-01
影响因子：
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通讯作者：
GORONZY, JJ
中科院分区：
文献类型：
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作者：
GOLD, KN;WEYAND, CM;GORONZY, JJ
目标。测定前列腺素对CD4+ T细胞产生白细胞介素2、4和5 （IL-2、IL-4和IL-5）、干扰素γ (IFN γ)、粒细胞-巨噬细胞集落刺激因子和转化生长因子β 1的影响。在前列腺素E(2) （PGE(2)）类似物米索前列醇和PGE(2)的存在和不存在的情况下，TH0、TH1和TH2 T细胞克隆均受到刺激。利用半定量聚合酶链反应和淋巴因子特异性引物组和/或通过生物测定测定淋巴因子活性来分析淋巴因子的产生。PGE(2)和米索前列醇对不同功能的T辅助细胞有不同的作用。主要产生IL-2和IFN γ的TH1细胞完全被抑制，而优先产生IL-4和IL-5的TH2细胞基本未受影响。米索前列醇和PGE(2)调节T细胞功能的能力是相同的。在前列腺素存在的情况下，TH2样辅助细胞，其特征是多种淋巴因子的共同产生，功能为TH2细胞；然而，它们不能分化为TH2 T细胞。炎症组织中产生的前列腺素可以调节浸润性T细胞的功能。在PGE存在的情况下(2)，th1样反应被抑制，th1样反应转向由IL-4和IL-5的产生主导的th2样模式。抗炎药抑制前列腺素的产生可能恢复TH1反应，局部产生IL-2和IFN γ。
Objective. To determine the influence of prostaglandins on the production of interleukins 2, 4, and 5 (IL-2, IL-4, and IL-5), interferon-gamma (IFN gamma), granulocyte-macrophage colony-stimulating factor, and transforming growth factor beta 1 by CD4+ T cells.Methods. TH0, TH1, and TH2 T cell clones were stimulated in the presence and absence of the prostaglandin E(2) (PGE(2)) 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 IFN gamma, 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 THO-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 IFN gamma.