A backhanded complement: Prostacyclin turns inflammation off from the inside out

IF 25.5 1区医学 Q1 IMMUNOLOGY

Immunity Pub Date : 2025-06-10 DOI:10.1016/j.immuni.2025.05.009

Samuel E.J. Preston, Russell G. Jones

引用次数: 0

Abstract

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 (PGI₂) signaling boosts interleukin (IL)-1R2 production to facilitate Th1 cell contraction.

查看原文本刊更多论文

一个反唇相讥的补充：前列环素可以从内到外消除炎症

为了限制过度活跃的辅助性T细胞（Th）1驱动的病理，这种T细胞群在病原体清除后收缩是至关重要的。在这一期的《免疫》杂志中，Rahman等人定义了一种补体- c5介导的脂类开关机制，该机制调节Th1自我控制。激活后，增强的细胞内源性前列腺环素（PGI2）信号会促进白细胞介素(IL)-1R2的产生，从而促进Th1细胞收缩。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Immunity 医学-免疫学

CiteScore

49.40

自引率

2.20%

发文量

205

审稿时长

6 months

期刊介绍： Immunity is a publication that focuses on publishing significant advancements in research related to immunology. We encourage the submission of studies that offer groundbreaking immunological discoveries, whether at the molecular, cellular, or whole organism level. Topics of interest encompass a wide range, such as cancer, infectious diseases, neuroimmunology, autoimmune diseases, allergies, mucosal immunity, metabolic diseases, and homeostasis.