一种拐弯抹角的赞美：前列环素从内而外抑制炎症。
A backhanded complement: Prostacyclin turns inflammation off from the inside out.
作者信息
Preston Samuel E J, Jones Russell G
机构信息
Department of Metabolism and Nutritional Programming, Van Andel Institute, Grand Rapids, MI, USA.
Department of Metabolism and Nutritional Programming, Van Andel Institute, Grand Rapids, MI, USA.
出版信息
Immunity. 2025 Jun 10;58(6):1361-1363. doi: 10.1016/j.immuni.2025.05.009.
To limit hyperactive T helper (Th)1-driven pathology, it is crucial that this T cell population contracts upon pathogen clearance. In this issue of Immunity, Rahman et al. define a complement-C5-mediated lipid-class-switch mechanism that regulates Th1 self-control. Following activation, enhanced cell-intrinsic prostacyclin (PGI) signaling boosts interleukin (IL)-1R2 production to facilitate Th1 cell contraction.
为了限制过度活跃的辅助性T细胞1（Th1）驱动的病理状况，至关重要的是，这种T细胞群体在病原体清除后会收缩。在本期《免疫》杂志中，拉赫曼等人确定了一种补体C5介导的脂质类别转换机制，该机制调节Th1的自我控制。激活后，增强的细胞内前列环素（PGI）信号传导会促进白细胞介素（IL）-1R2的产生，以促进Th1细胞的收缩。
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