• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

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。

相似文献

1
Cyclic AMP as a mediator of prostaglandin E-induced suppression of human natural killer cell activity.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。
J Immunol. 1983 Mar;130(3):1350-5.
2
PGE1 and prostacyclin suppression of NK-cell mediated cytotoxicity and its relation to cyclic AMP.
Med Biol. 1983;61(6):324-30.
3
Regulation of human natural cytotoxicity by IgG. II. Cyclic AMP as a mediator of monomeric IgG-induced inhibition of natural killer cell activity.
Cell Immunol. 1988 Jul;114(2):246-56. doi: 10.1016/0008-8749(88)90319-x.
4
Regulation of human natural killing. III. Mechanism for interferon induction of loss of susceptibility to suppression by cyclic AMP elevating agents.
J Immunol. 1984 Mar;132(3):1445-50.
5
Prostaglandin E2-induced changes in the phenotype, morphology, and lytic activity of IL-2-activated natural killer cells.前列腺素E2诱导的白细胞介素-2激活的自然杀伤细胞的表型、形态和裂解活性变化。
J Immunol. 1993 May 1;150(9):3747-54.
6
Effects of natural and recombinant IL 2 on regulation of IFN gamma production and natural killer activity: lack of involvement of the Tac antigen for these immunoregulatory effects.天然和重组白细胞介素2对γ干扰素产生调节及自然杀伤活性的影响:Tac抗原不参与这些免疫调节作用。
J Immunol. 1984 Aug;133(2):779-83.
7
Inhibition of bradykinin stimulation of renal medullary prostaglandin E2 synthesis by phosphodiesterase inhibitors.磷酸二酯酶抑制剂对缓激肽刺激肾髓质前列腺素E2合成的抑制作用。
J Pharmacol Exp Ther. 1981 Nov;219(2):442-6.
8
Modulation of human natural killer cell activity by pharmacological mediators.药理学介质对人类自然杀伤细胞活性的调节
Clin Exp Immunol. 1983 Nov;54(2):493-500.
9
The nature of the natural killer (NK) cell of human intestinal mucosa and mesenteric lymph node.人肠道黏膜和肠系膜淋巴结自然杀伤(NK)细胞的性质
Clin Exp Immunol. 1985 Jul;61(1):160-8.
10
Lysis of fresh human tumor cells by autologous large granular lymphocytes and T-lymphocytes: two distinct killing activities induced by coculture with autologous tumor.自体大颗粒淋巴细胞和T淋巴细胞对新鲜人肿瘤细胞的裂解作用:与自体肿瘤共培养诱导的两种不同杀伤活性。
J Natl Cancer Inst. 1984 Dec;73(6):1285-92.

引用本文的文献

1
Framework of Intrinsic Immune Landscape of Dormant Prostate Cancer.潜伏性前列腺癌固有免疫景观的框架。
Cells. 2022 May 5;11(9):1550. doi: 10.3390/cells11091550.
2
Antitumour immunity regulated by aberrant ERBB family signalling.异常 ERBB 家族信号调节的抗肿瘤免疫。
Nat Rev Cancer. 2021 Mar;21(3):181-197. doi: 10.1038/s41568-020-00322-0. Epub 2021 Jan 18.
3
Arachidonic Acid Derived Lipid Mediators Influence Kaposi's Sarcoma-Associated Herpesvirus Infection and Pathogenesis.花生四烯酸衍生的脂质介质影响卡波西肉瘤相关疱疹病毒的感染和发病机制。
Front Microbiol. 2019 Mar 12;10:358. doi: 10.3389/fmicb.2019.00358. eCollection 2019.
4
Tumor Microenvironment-Induced Immunometabolic Reprogramming of Natural Killer Cells.肿瘤微环境诱导自然杀伤细胞的免疫代谢重编程。
Front Immunol. 2018 Nov 8;9:2517. doi: 10.3389/fimmu.2018.02517. eCollection 2018.
5
Role of COX-2/PGE2 Mediated Inflammation in Oral Squamous Cell Carcinoma.COX-2/PGE2介导的炎症在口腔鳞状细胞癌中的作用
Cancers (Basel). 2018 Sep 22;10(10):348. doi: 10.3390/cancers10100348.
6
Understanding the tumour micro-environment communication network from an NOS2/COX2 perspective.从 NOS2/COX2 的角度理解肿瘤微环境通讯网络。
Br J Pharmacol. 2019 Jan;176(2):155-176. doi: 10.1111/bph.14488. Epub 2018 Nov 6.
7
Alveolar Macrophages in the Resolution of Inflammation, Tissue Repair, and Tolerance to Infection.肺泡巨噬细胞在炎症消退、组织修复和感染耐受中的作用。
Front Immunol. 2018 Jul 31;9:1777. doi: 10.3389/fimmu.2018.01777. eCollection 2018.
8
Growth and adherence of Staphylococcus aureus were enhanced through the PGE2 produced by the activated COX-2/PGE2 pathway of infected oral epithelial cells.感染的口腔上皮细胞激活的COX-2/PGE2途径产生的PGE2可增强金黄色葡萄球菌的生长和黏附。
PLoS One. 2017 May 4;12(5):e0177166. doi: 10.1371/journal.pone.0177166. eCollection 2017.
9
Macrophages and the Recovery from Acute and Chronic Inflammation.巨噬细胞与急慢性炎症的恢复
Annu Rev Physiol. 2017 Feb 10;79:567-592. doi: 10.1146/annurev-physiol-022516-034348. Epub 2016 Dec 7.
10
Implications of chemokine receptors and inflammatory lipids in cancer.趋化因子受体和炎性脂质在癌症中的意义
Immunotargets Ther. 2013 Dec 24;3:9-18. doi: 10.2147/ITT.S32049. eCollection 2014.