首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Increased splenocyte proliferative response and cytokine production in beta-endorphin-deficient mice.
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Increased splenocyte proliferative response and cytokine production in beta-endorphin-deficient mice.

机译:在β-内啡肽缺乏的小鼠中脾细胞增殖反应和细胞因子产生增加。

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摘要

We used beta-endorphin-deficient mice as a novel approach to confirm the physiological role that opioid peptides play in the development or regulation of the immune system. We found that mice lacking beta-endorphin possessed an enhanced immune response, measured in terms of splenocyte proliferation and interleukin (IL)-2 mRNA levels, in vitro production of the splenic macrophage inflammatory cytokines IL-6 and Tumor Necrosis Factor (TNF)-alpha and plasma IL-6 following lipopolysaccharide (LPS) administration. beta-Endorphin-deficient mice had attenuated increases of plasma ACTH and corticosterone levels in response to LPS. These results are consistent with a postulated inhibitory role of endogenous beta-endorphin on the immune system at multiple levels.
机译:我们使用β-内啡肽缺陷型小鼠作为一种新方法来确认阿片肽在免疫系统发育或调节中发挥的生理作用。我们发现缺乏β-内啡肽的小鼠具有增强的免疫反应,以脾细胞增殖和白介素(IL)-2 mRNA水平,脾脏巨噬细胞炎性细胞因子IL-6和肿瘤坏死因子(TNF)-的体外产生来衡量脂多糖(LPS)给药后的α和血浆IL-6。 β-内啡肽缺陷小鼠对LPS的反应减弱了血浆ACTH和皮质酮水平的升高。这些结果与内源性β-内啡肽在多个水平上对免疫系统的抑制作用相一致。

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