Vasoactive intestinal polypeptide suppressed experimental autoimmune encephalomyelitis by inhibiting T helper 1 responses
Vasoactive intestinal polypeptide suppressed experimental autoimmune encephalomyelitis by inhibiting T helper 1 responses
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DOI：
10.1007/s10875-006-9042-2
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发表时间：
2006-09-01
影响因子：
9.1
通讯作者：
Xu, Lingyun
中科院分区：
文献类型：
--
作者：
Li, Haiyan;Mei, Yunhua;Xu, Lingyun
血管活性肠肽(VIP)通过调节抗炎和促炎介质的产生，促进Th2型反应，是一种有效的抗炎因子。本研究采用髓鞘少突胶质细胞糖蛋白诱导的C57BL/6小鼠实验性自身免疫性脑脊髓炎(EAE)模型，探讨VIP对多发性硬化症的潜在作用。我们的结果表明，VIP对EAE诱导的小鼠在体治疗在临床和组织学水平上都有很大的保护作用。疾病抑制与抑制T细胞增殖、免疫反应向Th2型反应转变、影响促炎细胞因子如干扰素-γ、IL-6和IL-2以及趋化因子如RANTES的表达有关。综上所述，本研究提供了VIP通过抑制致病T细胞和通过对Th1应答的特异性作用而对EAE具有较强的保护作用的证据。
Vasoactive intestinal peptide (VIP) has been found to act as a potent anti-inflammatory factor through regulating the production of both anti- and pro-inflammatory mediators and promoting Th2-type responses. In this study, we used myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice to investigate the potential effects of VIP on multiple sclerosis. Our results showed that in vivo treatment of EAE-induced mice with VIP had great protective benefit at both clinical and histological levels. Disease suppression was associated with the inhibition of T cells proliferation, shifting of the immune response toward a Th2-type response and influencing the expression of pro-inflammatory cytokines including IFN-gamma, IL-6 and IL-2 as well as chemotactic factors such as RANTES. In conclusion, the study provides evidence that VIP had great protective effect on EAE through its inhibition actions on pathogenic T cells and through a specific effect on the Th1 response.