白细胞介素35在1型糖尿病中的保护作用及机制。

IF 1.5 4区 医学 Q4 IMMUNOLOGY Central European Journal of Immunology Pub Date : 2023-01-01 DOI:10.5114/ceji.2023.125043
Si-Ming Zhang, Jun Liang, Ji-Ping Xia, Li Li, Li Zheng, Ya-Lan Wang, Yan-Hong Li, Yan Li, Yu Lu
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引用次数: 1

摘要

白细胞介素35 (IL-35)是一种由调节性T细胞(Treg)从常规CD4+ T细胞分化而分泌的细胞因子,是IL-12家族的一员。IL-12家族细胞因子具有抗炎特性。IL-35最近被证明影响多种疾病的免疫调节,包括炎症性肠病、格雷夫斯病、类风湿性关节炎、结肠炎、牛皮癣和1型糖尿病(T1D)。T1D是一种由胰腺β细胞破坏引起的免疫相关疾病,其特征是绝对缺乏胰岛素。最近,研究表明IL-35的保护作用是通过改善血糖水平和防止胰岛炎症因子的攻击来发挥作用的。其保护机制可能与IL-35的抗炎特性密切相关,其抗炎特性包括调节巨噬细胞表型,抑制T细胞增殖,减少Th17细胞的分化,增加Treg细胞群,诱导产生IL-35的调节性T细胞(iTr35)。本文就IL-35在T1D中的保护作用及其机制进行综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Interleukin 35: protective role and mechanism in type 1 diabetes.

Interleukin 35 (IL-35), a cytokine secreted by regulatory T (Treg) cells from the differentiation of conventional CD4+ T cells, is a member of the IL-12 family. The IL-12 family of cytokines exhibits an anti-inflammatory property. IL-35 has recently been shown to influence the immune modulation in various diseases, including inflammatory bowel disease, Graves' disease, rheumatoid arthritis, colitis, psoriasis, and type 1 diabetes (T1D). T1D is an immune-related disease caused by destruction of pancreatic β cells, characterized by an absolute lack of insulin. Recently, studies have suggested that protective effects of IL-35 work by improving blood glucose levels and preventing an attack of inflammatory factors on the islets. The protective mechanism may be closely related to the anti-inflammatory properties of IL-35, which include regulating macrophage phenotype, suppressing T cell proliferation, decreasing the differentiation of Th17 cells, increasing the Treg cell population, and inducing IL-35-producing regulatory T cells (iTr35). Here, we review the protective effects and mechanisms of action of IL-35 in T1D.

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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
17
审稿时长
6-12 weeks
期刊介绍: Central European Journal of Immunology is a English-language quarterly aimed mainly at immunologists.
期刊最新文献
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