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Regulatory effect of vasoactive intestinal peptide on the balance of Treg and Th17 in collagen-induced arthritis.

机译:血管活性肠肽对胶原诱导的关节炎中Treg和Th17平衡的调节作用。

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摘要

Vasoactive intestinal peptide (VIP) is a well-known anti-inflammatory neuropeptide. The capacity of VIP can be exhibited through inhibiting inflammatory responses, shifting the Th1/Th2 balance in favor of anti-inflammatory Th2 immunity and inducing regulatory T cells (Tregs) with suppressive activity. In addition to pro-inflammatory Th1 response, Th17 are also believed to play important roles in the pathogenesis of rheumatoid arthritis (RA). In this study, we used collagen-induced arthritis (CIA) model in Wistar rats to investigate the role of VIP in the balance of CD4(+) CD25(+) Tregs and Th17 on RA. Data presented here showed that administration of VIP decreased incidence and severity of CIA. Disease suppression was associated with the upregulation of CD4(+) CD25(+) Tregs, downregulation of Th17- and Th1-type response and influence on the RANK/RANKL/OPG system. The results provide novel evidence that the therapeutic effects of VIP on CIA rats were associated with the balance of CD4(+) CD25(+) Tregs and Th17.
机译:血管活性肠肽(VIP)是众所周知的抗炎性神经肽。 VIP的能力可以通过抑制炎症反应,改变Th1 / Th2平衡以增强抗炎Th2免疫力以及诱导具有抑制活性的调节性T细胞(Tregs)来展现。除促炎性Th1反应外,Th17还被认为在类风湿关节炎(RA)的发病机理中起重要作用。在这项研究中,我们使用Wistar大鼠胶原诱导的关节炎(CIA)模型来研究VIP在RA中CD4(+)CD25(+)Treg和Th17平衡中的作用。此处提供的数据表明VIP的使用降低了CIA的发生率和严重程度。疾病抑制与CD4(+)CD25(+)Tregs的上调,Th17-型和Th1型应答的下调以及对RANK / RANKL / OPG系统的影响有关。结果提供了新的证据,表明VIP对CIA大鼠的治疗作用与CD4(+)CD25(+)Tregs和Th17的平衡有关。

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