Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children.
Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children.
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DOI：
10.1172/jci166016
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发表时间：
2023-01-03
影响因子：
15.9
通讯作者：
Arditi, Moshe
中科院分区：
文献类型：
--
作者：
Rivas, Magali Noval;Arditi, Moshe
儿童多系统炎症综合征（MIS-C）是一种罕见的儿童炎症性疾病，其特征是免疫细胞过度激活、细胞因子风暴和自身抗体的产生。这种免疫失调背后的机制仍然需要解开。在本期《JCI》中，Benamar等人证明了Notch受体1/CD22 （Notch1/CD22）轴在Treg中的关键作用，当其被激活时，会损害Treg功能并促进炎症。他们发现Notch1/CD22轴导致了MIS-C中失调的免疫反应。这些发现可能对MIS-C和许多其他炎症性疾病有启示。
Multisystem inflammatory syndrome in children (MIS-C) is a rare pediatric inflammatory disorder characterized by immune cell hyperactivation, cytokine storm, and the production of autoantibodies. The mechanisms underlying such immune dysregulation still need to be unraveled. In this issue of the JCI, Benamar et al. demonstrated the critical role of the Notch receptor 1/CD22 (Notch1/CD22) axis in Tregs, which, when activated, impairs Treg functions and promotes inflammation. They showed that the Notch1/CD22 axis contributed to dysregulated immune responses in MIS-C. These findings may have implications for MIS-C and many other inflammatory diseases.