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[儿茶酚胺对免疫功能调节的细胞和分子机制]

[Cellular and molecular mechanisms of regulation of immune functions by catecholamines].

作者信息

Qiu Yi-Hua, Peng Yu-Ping, Wang Jian-Jun

机构信息

Department of Biological Science and Technology, Nanjing University, Nanjing 210093.

出版信息

Sheng Li Ke Xue Jin Zhan. 2003 Oct;34(4):303-8.

Abstract

An increasing body of evidence suggests that catecholamines (CAs) do not only cause a general immunosuppression as previously believed, but suppress cellular immunity and boost humoral response. CAs can inhibit T helper 1 cells, T cytotoxic cells, natural killer cells and monocytes, but enhance T helper 2 cells and B cells through their direct regulation of these immune cells. In addition, CAs may modulate the gene transcription for cytokines in immune cells through stimulation of beta 2-adrenoreceptors and increase of cAMP, subsequently, activation of protein kinase A and alteration of the activity of nuclear transcription factors. Through these molecular mechanisms, the production of interleukin-2 (IL-2), tumor necrosis factor-alpha and IL-12 is decreased, but the production of IL-6, IL-10 and IL-4 is increased.

摘要

越来越多的证据表明,儿茶酚胺(CAs)并不像之前认为的那样仅引起全身性免疫抑制,而是会抑制细胞免疫并增强体液反应。CAs可抑制辅助性T1细胞、细胞毒性T细胞、自然杀伤细胞和单核细胞,但通过直接调节这些免疫细胞来增强辅助性T2细胞和B细胞。此外,CAs可能通过刺激β2 -肾上腺素能受体和增加环磷酸腺苷(cAMP),进而激活蛋白激酶A并改变核转录因子的活性,来调节免疫细胞中细胞因子的基因转录。通过这些分子机制,白细胞介素-2(IL-2)、肿瘤坏死因子-α和IL-12的产生减少,但IL-6、IL-10和IL-4的产生增加。

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