Acsbg1 regulates differentiation and inflammatory properties of CD4+ T cells

被引:0
|
作者
Palatella, Martina [1 ]
Kruse, Friederike [1 ]
Glage, Silke [2 ]
Bleich, Andre [2 ]
Greweling-Pils, Marina [3 ]
Huehn, Jochen [1 ,4 ]
机构
[1] Helmholtz Ctr Infect Res, Dept Expt Immunol, Inhoffenstr 7, D-38124 Braunschweig, Germany
[2] Hannover Med Sch, Inst Lab Anim Sci, Hannover, Germany
[3] Helmholtz Ctr Infect Res, Mouse Pathol Platform, Braunschweig, Germany
[4] Hannover Med Sch, Cluster Excellence RESIST EXC2155, Hannover, Germany
来源
EUROPEAN JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY | 2025年
基金
欧盟地平线“2020”;
关键词
Acsbg1; fatty acid metabolism; Th17; Treg; colitis; mucosal immunology; METABOLISM; LINEAGE; T(H)17; TH17; ALPHA;
D O I
10.1556/1886.2025.00003
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Epigenetic modifications are critical for the regulation of CD4+ T cell differentiation and function. Previously, we identified Acyl-CoA Synthetase Bubble Gum 1 (Acsbg1), a gene involved in fatty acid metabolism, as part of an epigenetic signature that was selectively demethylated in ex vivo isolated T helper 17 (TH17) cells. However, its functional relevance for CD4+ T cells remains incompletely understood. Here, we used in vitro differentiation assays and the adoptive transfer colitis model to investigate the role of Acsbg1 in the differentiation and function of TH1, TH17, and regulatory T (Treg) cells. In vitro, Acsbg1 was expressed in both TH17 and in vitro-induced Treg (iTreg) cells, whereas TH1 cells lacked Acsbg1 expression. Accordingly, Acsbg1 deficiency resulted in impaired TH17 and iTreg differentiation, whereas TH1 differentiation was unaffected. In vivo, upon adoptive transfer of Acsbg1(-)/(-) Tna & iuml;ve cells, immunodeficient recipient mice exhibited an exacerbated colitis, characterized by an altered balance of TH17 and Treg cells, indicating that Acsbg1 expression is essential for optimal TH17 and Treg cell differentiation and function. Our findings highlight the importance of fatty acid (FA) metabolism in maintaining immune homeostasis by regulating T cell differentiation and provide novel insights into the metabolic targeting of inflammatory diseases.
引用
收藏
页数:11
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