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在和肠道炎症中准T细胞可塑性,通过聚合单细胞CRISPR查

Leon U B Enk^1,2,3, Malte Hellmig^1,2,3, Kristoffer Riecken⁴

¹III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Science immunology

|June 14, 2024

概括

研究人员发现T助手17 (T_H17) 细胞在脏自身免疫中的可塑性. 这一发现可以通过向T细胞两极分化来治疗自身免疫性疾病的新疗法.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
遗传学遗传学是一种遗传学.

背景情况:

支持炎症的CD4+T细胞,特别是T辅助细胞17 (T_H17),是自身免疫性疾病的关键驱动因素.
目前的疗法缺乏有效调节T细胞表型到抗炎状态的能力.

研究的目的:

在自身免疫环境中识别T细胞两极化和可塑性的分子驱动因素.
为了研究T_H17细胞在自身免疫性质炎期间在脏微环境中的可塑性.

主要方法:

利用单细胞T细胞受体测序和scRNA速度来分析患者的T细胞群.
在小鼠模型中开发并应用了体内聚合的scCRISPR滴滴测序 (iCROP-seq) 屏幕.
量化T_H17细胞对T辅助1 (T_H1) 和调节性T细胞的偏向.

主要成果:

鉴定了T_H17细胞在患有抗中性粒细胞质抗体相关的球隆炎的患者的脏中的可塑性.
证明iCROP-seq可以根据转录变化对T_H17细胞中基于CRISPR的基因扰动进行排序.
展示了iCROP-seq通过功能基因和途径分层识别治疗点的能力.

结论:

在自身免疫期间,在人类脏中发现了T_H17到T_H1细胞可塑性.
建立了iCROP-seq作为一种强大的工具,用于发现T细胞介导的自身免疫性疾病中的疾病和组织特异性治疗点.
为开发针对自身免疫性疾病中T细胞可塑性的新型免疫疗法提供了基础.

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