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环磷酸腺苷作为前列腺素E诱导人自然杀伤细胞活性抑制的介质。

Cyclic AMP as a mediator of prostaglandin E-induced suppression of human natural killer cell activity.

作者信息

Goto T, Herberman R B, Maluish A, Strong D M

出版信息

J Immunol. 1983 Mar;130(3):1350-5.

PMID:6185577
Abstract

The role of cyclic AMP in mediating the prostaglandin (PG) E2-induced suppression of natural killer (NK) cell function was studied. Highly purified preparations of human large granular lymphocytes (LGL; which have been shown to be closely associated with human NK activity) and T lymphocytes were obtained by using Percoll gradients. Basal cyclic AMP was similar in both cell populations. With LGL, PGE2 (but not PGF2 alpha) suppressed NK activity (75%) and enhanced cellular cycle AMP (600%). In contrast, in small, high density T lymphocytes, PGE2 caused very small increases in cyclic AMP (20%). Phosphodiesterase inhibitors (PDEI) such as isobutyl methylxanthine and theophylline also increased cyclic AMP and suppressed NK activity in LGL. The effect of PGE2 and PDEI, in combination on cellular cyclic AMP and NK activity, was greater than the effect of each agent alone. Finally, exogenous derivatives of cyclic AMP also suppressed NK activity. These results indicate that in LGL, increased cellular cyclic AMP mediates the action of PGE2 on the suppression of NK activity.

摘要

研究了环磷酸腺苷(cAMP)在介导前列腺素(PG)E2诱导的自然杀伤(NK)细胞功能抑制中的作用。通过使用Percoll梯度获得了高度纯化的人大颗粒淋巴细胞(LGL;已证明其与人类NK活性密切相关)和T淋巴细胞制剂。两种细胞群体中的基础cAMP相似。对于LGL,PGE2(而非PGF2α)抑制NK活性(75%)并增强细胞内cAMP(600%)。相比之下,在小的高密度T淋巴细胞中,PGE2导致cAMP的增加非常小(20%)。磷酸二酯酶抑制剂(PDEI)如异丁基甲基黄嘌呤和茶碱也增加cAMP并抑制LGL中的NK活性。PGE2和PDEI联合对细胞内cAMP和NK活性的影响大于每种药物单独的作用。最后,cAMP的外源性衍生物也抑制NK活性。这些结果表明,在LGL中,细胞内cAMP的增加介导了PGE2对NK活性抑制的作用。

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