IL-35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells.
IL-35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells.
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IL-35重组蛋白通过调节炎症细胞因子和免疫细胞逆转炎症性肠病和牛皮癣
DOI：
10.1111/jcmm.13428
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发表时间：
2018-03
影响因子：
5.3
通讯作者：
Deng H
中科院分区：
文献类型：
--
作者：
Wang Y;Mao Y;Zhang J;Shi G;Cheng L;Lin Y;Li Y;Zhang X;Zhang Y;Chen X;Deng J;Su X;Dai L;Yang Y;Zhang S;Yu D;Wei Y;Deng H
白细胞介素-35（IL-35）是IL-12家族的一员，是一种新的抗炎因子，参与关节炎、银屑病、炎症性肠病（IBD）等免疫性疾病。虽然IL-35可以显著预防许多疾病中的炎症发展，但尚未有早期研究说明IL-35重组蛋白在IBD和银屑病中的作用。在这项研究中，我们评估了IL-35重组蛋白在三种众所周知的小鼠模型中的治疗潜力：右旋糖酐硫酸钠（DSS）诱导的结肠炎小鼠模型，角蛋白14（K14）-血管内皮生长因子A（VEGF-A）-转基因（Tg）银屑病小鼠模型和咪喹莫特（IMQ）诱导的银屑病小鼠模型。我们的结果表明，IL-35重组蛋白可以通过减少巨噬细胞、CD 4 +T和CD 8 +T细胞的浸润以及通过促进Treg细胞的浸润来减缓DSS诱导的急性结肠炎小鼠模型的病理过程。进一步分析表明，IL-35重组蛋白可能通过促进IL-10的分泌和抑制促炎细胞因子如IL-6、TNF-α和IL-17的表达来调节急性结肠炎模型中的炎症。此外，在银屑病小鼠中，较低剂量的IL-35重组蛋白可以达到与TNF-α单克隆抗体相同的长期治疗效果。综上所述，IL-35重组蛋白在急性结肠炎和银屑病小鼠模型中的显著治疗效果表明，IL-35重组蛋白具有多种抗炎作用，有望成为治疗炎症性疾病的有效候选药物。
Interleukin‐35 (IL‐35), a member of the IL‐12 family, functions as a new anti‐inflammatory factor involved in arthritis, psoriasis, inflammatory bowel disease (IBD) and other immune diseases. Although IL‐35 can significantly prevent the development of inflammation in many diseases, there have been no early studies accounting for the role of IL‐35 recombinant protein in IBD and psoriasis. In this study, we assessed the therapeutic potential of IL‐35 recombinant protein in three well‐known mouse models: the dextransulfate sodium (DSS)‐induced colitis mouse model, the keratin14 (K14)‐vascular endothelial growth factor A (VEGF‐A)‐transgenic (Tg) psoriasis mouse model and the imiquimod (IMQ)‐induced psoriasis mouse model. Our results indicated that IL‐35 recombinant protein can slow down the pathologic process in DSS‐induced acute colitis mouse model by decreasing the infiltrations of macrophages, CD4+T and CD8+T cells and by promoting the infiltration of Treg cells. Further analysis demonstrated that IL‐35 recombinant protein may regulate inflammation through promoting the secretion of IL‐10 and inhibiting the expression of pro‐inflammatory cytokines such as IL‐6, TNF‐α and IL‐17 in acute colitis model. In addition, lower dose of IL‐35 recombinant protein could achieve long‐term treatment effects as TNF‐α monoclonal antibody did in the psoriasis mouse. In summary, the remarkable therapeutic effects of IL‐35 recombinant protein in acute colitis and psoriasis mouse models indicated that IL‐35 recombinant protein had a variety of anti‐inflammatory effects and was expected to become an effective candidate drug for the treatment of inflammatory diseases.
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