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首页> 美国卫生研究院文献>Arthritis Research >Induction of IL-10-producing CD4+CD25+ T cells in animal model of collagen-induced arthritis by oral administration of type II collagen
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Induction of IL-10-producing CD4+CD25+ T cells in animal model of collagen-induced arthritis by oral administration of type II collagen

机译：通过口服II型胶原诱导胶原诱导的关节炎动物模型中产生IL-10的CD4 + CD25 + T细胞的诱导

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Induction of oral tolerance has long been considered a promising approach to the treatment of chronic autoimmune diseases, including rheumatoid arthritis (RA). Oral administration of type II collagen (CII) has been proven to improve signs and symptoms in RA patients without troublesome toxicity. To investigate the mechanism of immune suppression mediated by orally administered antigen, we examined changes in serum IgG subtypes and T-cell proliferative responses to CII, and generation of IL-10-producing CD4+CD25+ T-cell subsets in an animal model of collagen-induced arthritis (CIA). We found that joint inflammation in CIA mice peaked at 5 weeks after primary immunization with CII, which was significantly less in mice tolerized by repeated oral feeding of CII before CIA induction. Mice that had been fed with CII also exhibited increased serum IgG1 and decreased serum IgG2a as compared with nontolerized CIA animals. The T-cell proliferative response to CII was suppressed in lymph nodes of tolerized mice also. Production of IL-10 and of transforming growth factor-β from mononuclear lymphocytes was increased in the tolerized animals, and CD4+ T cells isolated from tolerized mice did not respond with induction of IFN-γ when stimulated in vitro with CII. We also observed greater induction of IL-10-producing CD4+CD25+ subsets among CII-stimulated splenic T cells from tolerized mice. These data suggest that when these IL-10-producing CD4+CD25+ T cells encounter CII antigen in affected joints they become activated to exert an anti-inflammatory effect.
机译：长期以来，诱导口服耐受一直被认为是治疗包括类风湿关节炎（RA）在内的慢性自身免疫疾病的一种有前途的方法。口服II型胶原蛋白（CII）已被证明可以改善RA患者的体征和症状，而不会产生毒性。为了研究口服抗原介导的免疫抑制机制，我们研究了血清IgG亚型和对CII的T细胞增殖反应的变化，以及产生IL-10-的CD4 + CD25 的产生。胶原诱导的关节炎（CIA）动物模型中的+ T细胞亚群。我们发现CIA小鼠的关节发炎在用CII初次免疫后5周达到高峰，而在CIA诱导前反复口服CII耐受的小鼠中的关节发炎明显更少。与未耐受的CIA动物相比，用CII喂养的小鼠还表现出血清IgG1升高和血清IgG2a降低。耐受小鼠的淋巴结也抑制了对CII的T细胞增殖反应。在耐受的动物中，单核淋巴细胞产生IL-10和转化生长因子-β的量增加，并且在刺激下，从耐受的小鼠分离的CD4 + T细胞对IFN-γ的诱导没有反应。 CII体外。我们还观察到在耐受小鼠的CII刺激的脾T细胞中，IL-10产生的CD4 + CD25 + 亚集的诱导作用更大。这些数据表明，当这些产生IL-10的CD4 + CD25 + T细胞在受影响的关节中遇到CII抗原时，它们就被激活以发挥抗炎作用。

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