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在1型糖尿病中,USP7在调节宽容性树突细胞功能的作用

Farhan Ullah Khan¹, Puregmaa Khongorzul¹, Denis Gris²

¹Department of Pediatrics, Immunology Division, Université de Sherbrooke Faculté de Médecine et des Sciences de la Santé, 3001, 12 th Avenue North, Sherbrooke, QC, J1H 5 N4, Canada.

Cellular & molecular biology letters

|April 17, 2025

概括

在NOD小鼠中,USP7/Ezh2轴对维持能耐性树突细胞 (toDCs) 至关重要,这些细胞可以保护NOD小鼠免受1型糖尿病 (T1D) 的侵害. 抑制USP7会破坏这些toDCs,导致糖尿病发病.

科学领域:

免疫学免疫学免疫学
内分泌学在内分泌学.
细胞生物学细胞生物学

背景情况:

宽容性树突细胞 (toDCs) 对于免疫常态稳定和预防1型糖尿病 (T1D) 等自身免疫性疾病至关重要.
在非肥胖糖尿病 (NOD) 小鼠的树突细胞 (DC) 中激活Stat5b,赋予了toDC特征,并保护糖尿病.
控制DC重编程到宽容性或免疫性表型的精确机制仍然不完全理解.

研究的目的:

在T1D的背景下,研究USP7在DC介导免疫调节中的作用.
阐明Stat5b在转基因NOD小鼠模型中影响DC功能和耐受性的机制.

主要方法:

从NOD和NOD.Stat5b-CA小鼠使用流动细胞计 (FACS) 和西部斑点的 DCs的分析.
评估细胞因子概况,转录因子 (IRF4,IRF8),USP7和Ezh2表达.
在体内直流转移模型评估USP7抑制对T细胞反应和糖尿病发病的影响.

主要成果:

与NOD DC相比,Stat5b-CA.DCs表现出更高的USP7,Ezh2和PD-L1/2表达,具有较高比例的宽容性cDC2子集.
在Stat5b-CA.DC中USP7阻断促进了成熟,促炎性细胞因子和cDC1亚群分化,同时减少了抗炎性细胞因子和PD-L1/2.2.
在NOD小鼠中,USP7抑制逆转了Stat5b-CA.DCs的保护作用,导致糖尿病发病.

结论:

USP7/Ezh2轴在维持DCs的耐受性功能方面发挥着重要作用.
这些功能对于调节自适应性免疫反应和在NOD小鼠中给予糖尿病保护至关重要.

关键词:

树状细胞树状细胞在 Ezh2 2 中.免疫治疗是一种免疫疗法.在PD-L1/2 第1类糖尿病患者.USP7 USP7 美国

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