Goodwin J S, Ceuppens J
J Clin Immunol. 1983 Oct;3(4):295-315. doi: 10.1007/BF00915791.
Of all the arachidonic acid metabolites, only prostaglandin E (PGE) has been shown to have a clear role in the regulation of cellular and humoral immune responses. In cellular immune responses such as T cell proliferation, lymphokine production, and cytotoxicity, PGE usually acts as a feedback inhibitor of the response. This is also true of macrophage and natural killer cytotoxicity. In some instances PGE is responsible for cellular activation rather than inhibition. This is clearest in the control of humoral immunity, where PGE production is a necessary component in the generation of some type of T suppressor cells. Disturbances in immune function found in several human conditions and diseases have been linked to changes in PGE mediated immunoregulation. Either increased production of PGE or increased sensitivity to PGE results in depressed cellular immunity. Conversely drugs which inhibit PGE production act as stimulants of cellular immune function in vitro and in vivo.
在所有花生四烯酸代谢产物中,只有前列腺素E(PGE)已被证明在调节细胞免疫和体液免疫反应中具有明确作用。在细胞免疫反应中,如T细胞增殖、淋巴因子产生和细胞毒性作用,PGE通常作为反应的反馈抑制剂。巨噬细胞和自然杀伤细胞的细胞毒性作用也是如此。在某些情况下,PGE负责细胞激活而非抑制。这在体液免疫控制中最为明显,其中PGE的产生是某些类型抑制性T细胞生成的必要组成部分。在几种人类病症和疾病中发现的免疫功能紊乱与PGE介导的免疫调节变化有关。PGE产生增加或对PGE敏感性增加都会导致细胞免疫抑制。相反,抑制PGE产生的药物在体外和体内均作为细胞免疫功能的刺激剂。