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Neuroimmune Regulation in Immunocompetence, Acute Illness, and Healing

机译:免疫振动,急性疾病和愈合的神经影响调节

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Adaptive immunocompetence is maintained by growth hormone (GH), prolactin (PRL),and vasopressin (VP). Innate or natural immunocompetence depends on cytokines, hor-mones (especially of the hypothalamus—pituitary—adrenal axis), and catecholamines.The acute phase response (APR, or acute febrile illness) is an emergency defense re-action whereby the adaptive, T cell—dependent, immune reactions are suppressed andthe innate immune function is dramatically amplified. Infection and various forms ofinjury induce APR. Cytokines [interleukin (M)-1β, tumor necrosis factor-a, and IL-6]stimulate corticotropin-releasing hormone (CRH) and VP secretion and cause a "sym-pathetic outflow." Colony-stimulating factors activate leukocytes. CRH is a powerfulactivator of the pituitary adrenocortical axis and elevates glucocorticoid (GC) levels.Cytokines, GCs, and catecholamines play fundamental roles in the amplification of nat-ural immune defense mechanisms. VP supports the APR at this stage. However, VPremains active and is elevated for a longer period than is CRH. VP, but not CRH, iselevated during chronic inflammatory diseases. VP controls adaptive immune functionand stimulates adrenocorticotropic hormone (ACTH) and PRL secretion. PRL main-tains the function of the thymus and of the T cell—dependent adaptive immune system.The ACTH—adrenal axis stimulates natural immunity and of suppressor/regulatory Tcells, which suppress the adaptive immune system. VP also has a direct effect on lym-phoid cells, the significance of which remains to be elucidated. It is suggested that VPregulates the process of recovery from acute illness.
机译:通过生长激素(GH),催乳素(PRL)和血管加压素(VP)维持自适应免疫合作症。天生或天生的免疫功能性依赖于细胞因子,Hor-Mones(特别是丘脑 - 垂体 - 肾上腺轴),以及儿茶酚胺。急性期反应(APR或急性发热疾病)是一种紧急防御重新行动,由此适应,T抑制细胞依赖性,免疫反应,并急剧扩增天生的免疫功能。感染和各种形式的OFINJURY诱导4月。细胞因子[白细胞介素(M)-1β,肿瘤坏死因子-α和IL-6]刺激皮质甾醇释放激素(CRH)和VP分泌,并导致“敏感性流出。”。殖民地刺激因子激活白细胞。 CRH是垂体肾上腺皮质轴的强效器,升高糖皮质激素(GC)水平。胞内因子,GCS和儿茶酚胺在扩增NAT-utal免疫防御机制中起着基本作用。 VP在此阶段支持APR。然而,vpremains活跃并且升高比CRH更长。 VP,但不是CRH,在慢性炎症性疾病期间缺乏。 VP控制自适应免疫功能和刺激肾上腺皮质激素(ACTH)和PRL分泌。 PRL主要抑制胸腺和T细胞依赖性自适应免疫系统的功能。Acth - 肾上腺轴刺激自然免疫和抑制/调节TCells,抑制了自适应免疫系统。 VP还对Lym-Phoid细胞的直接影响,其意义仍有待阐明的。建议v培养从急性疾病中恢复的过程。

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