小柯机器人

中山大学施松涛等研究人员合作发现，细胞凋亡释放硫化氢来抑制Th17细胞分化。这一研究成果于2023年12月18日在线发表在国际学术期刊《细胞—代谢》上。

研究人员发现凋亡缺陷的MRL/lpr（B6.MRL-Faslpr/J）和Bim^-/-（B6.129S1-Bcl2l11tm1.1Ast/J）小鼠表现出明显的硫化氢（H₂S）水平降低和Th17细胞的异常分化，这可以通过额外的H₂S来挽救。此外，凋亡细胞和囊泡（apoV）表达关键的H₂S生成酶，并生成大量H₂S，这表明凋亡代谢是H₂S的重要来源。

从机理上讲，H₂S修饰硒蛋白F（Sep15），促进信号转导和转录激活因子1（STAT1）磷酸化，抑制STAT3磷酸化，从而抑制Th17细胞分化。综上所述，这项研究揭示了细胞凋亡在维持H₂S稳态中的一种未知作用，以及H₂S通过修饰Sep15^C38在调节Th17细胞分化中的独特作用。

据介绍，成人体内每天有超过500亿个细胞凋亡，以维持免疫平衡。H₂S也是保障免疫反应功能所需的。然而，细胞凋亡是否能调节H₂S的产生还不得而知。

附：英文原文

Title: Apoptosis releases hydrogen sulfide to inhibit Th17 cell differentiation

Author: Qianmin Ou, Xinhua Qiao, Zhengshi Li, Luhan Niu, Fangcao Lei, Ruifeng Cheng, Ting Xie, Ning Yang, Yao Liu, Ling Fu, Jing Yang, Xueli Mao, Xiaoxing Kou, Chang Chen, Songtao Shi

Issue&Volume: 2023-12-18

Abstract: Over 50 billion cells undergo apoptosis each day in an adult human to maintain immune homeostasis. Hydrogen sulfide (H2S) is also required to safeguard the function of immune response. However, it is unknown whether apoptosis regulates H2S production. Here, we show that apoptosis-deficient MRL/lpr (B6.MRL-Faslpr/J) and Bim/ (B6.129S1-Bcl2l11tm1.1Ast/J) mice exhibit significantly reduced H2S levels along with aberrant differentiation of Th17 cells, which can be rescued by the additional H2S. Moreover, apoptotic cells and vesicles (apoVs) express key H2S-generating enzymes and generate a significant amount of H2S, indicating that apoptotic metabolism is an important source of H2S. Mechanistically, H2S sulfhydrates selenoprotein F (Sep15) to promote signal transducer and activator of transcription 1 (STAT1) phosphorylation and suppress STAT3 phosphorylation, leading to the inhibition of Th17 cell differentiation. Taken together, this study reveals a previously unknown role of apoptosis in maintaining H2S homeostasis and the unique role of H2S in regulating Th17 cell differentiation via sulfhydration of Sep15C38.

DOI: 10.1016/j.cmet.2023.11.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00444-8

Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
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