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在捐赠者T细胞中SOCS1的损失通过驱动一种依赖于化学的亲炎性免疫微环境,加剧了肠道GVHD

Zhigui Wu^1,2, Bixia Wang¹, Xinya Jiang¹

¹Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|January 25, 2026

概括

在T细胞中抑制细胞因子信号传递1 (SOCS1) 损失通过促进炎症驱动致命的移植对宿主疾病 (GVHD). JAK1/2抑制和高SOCS1表达预测了更好的结果,将SOCS1确定为治疗点.

科学领域:

免疫学免疫学免疫学
血液学血液学血液学
在瘤学瘤学.

背景情况:

急性移植对宿主疾病 (aGVHD) 是全源造血干细胞移植的主要并发症.
抑制细胞因子信号传递1 (SOCS1) 在T细胞介导的aGVHD病原体中的作用尚未完全理解.

研究的目的:

为了研究SOCS1在aGVHD.期间在T细胞中的内在作用.
确定SOCS1作为潜在的治疗标和aGVHD.生物标记物.

主要方法:

使用T细胞特异的Socs1淘汰赛小鼠模型.
分析了T细胞分化,基因表达 (Ccl5),免疫细胞透 (单细胞,巨细胞) 和移植后的组织损伤.
评估了JAK1/2抑制 (鲁克索利提尼布) 的疗效.
与临床aGVHD发病率相关的SOCS1表达.

主要成果:

在T细胞,特别是CD8+T细胞中的Socs1损失促进了促炎分化和STAT1/2-依赖的Ccl5表达.
缺少Socs1的T细胞表现出增强的肠道透,增加的CD8+T细胞效应因子功能,以及炎症性巨细胞两极分化.
这些变化导致严重的组织损伤和致命的aGVHD.
卢克索利提尼布治疗逆转了这些致病效应.
在CD8+ T细胞中高供体SOCS1表达与降低aGVHD发病率相关.

结论:

在T细胞中内在的SOCS1缺乏驱动致命的aGVHD病原体.
在aGVHD.中,SOCS1充当T细胞反应的关键调节者.
抑制JAK1/2是一种有前途的治疗策略.
SOCS1是个性化aGVHD预防的潜在预测生物标志物.

关键词:

骨髓移植骨髓移植细胞迁移细胞迁移化学物质是化学物质,化学物质是化学物质.胃肠道的胃肠道是什么肠道T细胞是指肠道T细胞.

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