期刊
IMMUNITY
卷 54, 期 8, 页码 1728-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2021.07.004
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类别
资金
- National Key R&D Program of China [2018YFA0800503]
- Excellent Young Scientist Fund of NSFC [31822017]
- Zhejiang Provincial Natural Science Foundation of China [LR19C080001]
- National Natural Science Foundation of China [81771675, 81970484]
- Key R&D Program of Zhejiang Province [2020C03075]
In this study, the researchers examined the immunological features and metabolic microenvironment of untreated individuals with IBD and found that selenium plays a crucial role in regulating T cell responses in CD. Selenium supplementation can alleviate CD symptoms by suppressing Th1 cell differentiation. This highlights selenium as a potential therapeutic target in CD.
Inflammatory bowel disease (IBD) mainly includes Crohn's disease (CD) and ulcerative colitis (UC). Immune disorders play an essential role in the pathogenesis of these two IBDs, but the differences in the immune microenvironment of the colon and their underlying mechanisms remain poorly investigated. Here we examined the immunological features and metabolic microenvironment of untreated individuals with IBD by multiomics analyses. Modulation of CD-specific metabolites, particularly reduced selenium, can obviously shape type 1 T helper (Th1) cell differentiation, which is specifically enriched in CD. Selenium supplementation suppressed the symptoms and onset of CD and Th1 cell differentiation via selenoprotein W (SELW)-mediated cellular reactive oxygen species scavenging. SELW promoted purine salvage pathways and inhibited one-carbon metabolism by recruiting an E3 ubiquitin ligase, tripartite motif-containing protein 21, which controlled the stability of serine hydroxymethyltransferase 2. Our work highlights selenium as an essential regulator of T cell responses and potential therapeutic targets in CD.
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