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促肾上腺皮质激素释放激素与免疫系统。

CRH and the immune system.

作者信息

Karalis K, Muglia L J, Bae D, Hilderbrand H, Majzoub J A

机构信息

Division of Endocrinology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

出版信息

J Neuroimmunol. 1997 Feb;72(2):131-6. doi: 10.1016/s0165-5728(96)00178-6.

Abstract

Inflammatory cytokines released during immune system activation can stimulate the hypothalamic-pituitary-adrenal axis and cause increased secretion of corticotropin-releasing hormone (CRH), adrenocorticotropin and glucocorticoids. Identification of CRH peptide and mRNA, as well as its receptors in immune tissues, suggested a role for this peptide as a mediator of the neuroendocrine-immune interactions. Experimental evidence suggests that CRH may modulate the immune and inflammatory responses via two pathways: an antiinflammatory one operated by centrally released CRH, most likely through stimulation of glucocorticoid and catecholamine release, and one proinflammatory, through direct action of peripherally released CRH. This review highlights these concepts. In addition preliminary data on immune activation and inflammatory response in CRH-deficient mice created in our laboratory are discussed.

摘要

免疫系统激活过程中释放的炎性细胞因子可刺激下丘脑-垂体-肾上腺轴,导致促肾上腺皮质激素释放激素(CRH)、促肾上腺皮质激素和糖皮质激素分泌增加。在免疫组织中鉴定出CRH肽及其mRNA以及其受体,提示该肽作为神经内分泌-免疫相互作用的介质发挥作用。实验证据表明,CRH可能通过两条途径调节免疫和炎症反应:一条是由中枢释放的CRH介导的抗炎途径,很可能是通过刺激糖皮质激素和儿茶酚胺释放来实现;另一条是促炎途径,通过外周释放的CRH的直接作用来实现。本综述重点介绍了这些概念。此外,还讨论了我们实验室培育的CRH缺陷小鼠免疫激活和炎症反应的初步数据。

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