Mechanisms of immune suppression for activated T cells by infliximab therapy in patients with Behcet's uveoretinitis.

既往研究表明，Behcet病（BD）的眼内炎症以Th1和Th17免疫应答为主。最近，Th22细胞被鉴定为与自身免疫性疾病相关的一种新的Th谱系。我们发现从BD患者的眼部样本中建立的th22型T细胞克隆产生大量的th22相关细胞因子IL-22和TNF-α。BD患者外周血中CD4+ T细胞分化为Th22细胞。暴露于抗tnf -α抗体英夫利昔单抗的Th22细胞体外不能产生IL-22。此外，从患有实验性自身免疫性葡萄膜炎（一种BD动物模型）的小鼠中分离出Th22细胞，在视网膜抗原存在的情况下，来自EAU的眼内T细胞产生大量IL-22。这些结果提示Th22细胞可能在BD患者的眼部炎症中起关键作用，英夫利昔单抗抑制Th22细胞可能保护眼膜炎患者免受严重的眼部炎症。

Previous studies suggested that the intraocular inflammation in Behcet’s disease (BD) is predominated by Th1 and Th17 immune responses. Recently, Th22 cells were identified as a novel Th lineage associated with autoimmune diseases. We showed that Th22-type T cell clones established from ocular samples from patients with BD produced large amounts ofTh22 associated cytokines IL-22 and TNF-α. CD4+ T cells from PBMCs of BD patients differentiated into Th22 cells. Th22 cells exposed to infliximab, anti-TNF-αantibody, in vitro failed to produce IL-22. Moreover, Th22 cells were isolated from mice with experimental autoimmune uveitis (EAU), an animal model of BD, and intraocular T cells from EAU produced large amounts of IL-22 in the presence of retinal antigens. Theseresults suggest that Th22 cells may play a key role in the ocular inflammation in BD. Suppression of Th22 cells by infliximab may protect uveitis patients with BD from severe ocular inflammation.