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Neuronal Modulation Of The Immune Response

机译:免疫反应的神经元调节

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The nervous and immune systems respond in distinct manners to diverse signals. Crosstalk between these systems has been known: microbial infections can result in inflammation of nervous tissue and lead to conditions such as encephalitis and meningitis. Also, the immune response causes damage to nervous tissue during autoimmune diseases: extensive axonal damage is observed in multiple sclerosis due to demyelination and infiltration by leukocytes (Mix et al 2007). To study the roles of immune molecules, researchers often use a mouse model of multiple sclerosis known as experimental autoimmune encephalomyelitis in which disease is induced upon injection of myelin oligodendrocyte glycoprotein in Complete Freund's adjuvant. Here, inflammatory cytokines, e.g. Interferon-y (Tran et al 2000) and Tumour necrosis Factor-α (Liu et al 1998), or Toll-like receptors (TLR)-4 or TLR-9, which detect microbial constituents (Marta et al 2008), play regulatory roles to reduce disease severity. In cases like these, it is not too surprising that inflammatory immune molecules affect nervous tissues. On the other hand, proper understanding is lacking on how neuronal products modulate immune reactions, especially with respect to anti-pathogen responses.
机译:神经和免疫系统以不同的方式响应各种信号。这些系统之间的串扰是众所周知的:微生物感染会导致神经组织发炎,并导致诸如脑炎和脑膜炎等疾病。同样,免疫反应会在自身免疫疾病期间对神经组织造成损害:由于脱髓鞘和白细胞浸润,在多发性硬化症中观察到了广泛的轴突损害(Mix等,2007)。为了研究免疫分子的作用,研究人员经常使用称为实验性自身免疫性脑脊髓炎的多发性硬化症小鼠模型,其中在完全弗氏佐剂中注射髓磷脂少突胶质细胞糖蛋白会诱发疾病。在此,炎性细胞因子例如干扰素-γ(Tran等,2000)和肿瘤坏死因子-α(Liu等,1998)或检测微生物成分的Toll样受体(TLR)-4或TLR-9(Marta等,2008)发挥调节作用降低疾病严重程度的作用。在这种情况下,炎症性免疫分子影响神经组织也就不足为奇了。另一方面,对于神经元产物如何调节免疫反应,尤其是在抗病原体反应方面,缺乏适当的了解。

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