胃肠道(GI)氧化还原环境,受共生微生物群和细菌衍生代谢物的影响,对形成T细胞反应至关重要。具体来说,来自肠道微生物群(GM)的代谢物表现出强大的抗炎作用,促进CD8+组织驻留记忆(TRM)细胞的分化和调节,粘膜相关不变T(MAIT)细胞,和稳定肠道驻留的Treg细胞。一氧化氮(NO),一个关键的氧化还原介质,作为T细胞功能和肠道炎症的中枢调节剂出现。NO影响肠道微生物组的组成,驱动促炎Th17细胞的分化并加剧肠道炎症,并支持Treg扩展,展示其在免疫稳态中的双重作用。这篇综述深入研究了GI氧化还原平衡和GM代谢物之间复杂的相互作用,阐明它们对T细胞调节的深远影响。此外,它全面强调了胃肠道氧化还原的关键作用,特别是活性氧(ROS)和NO,塑造T细胞表型和功能。这些见解为与氧化应激相关的疾病机制和潜在治疗策略提供了有价值的观点。了解GI氧化还原之间的复杂串扰,转基因代谢物,T细胞反应为免疫介导疾病的潜在治疗途径提供了有价值的见解,强调维持GI氧化还原平衡对最佳免疫健康的重要性。
The gastrointestinal (GI) tract
redox environment, influenced by commensal microbiota and bacterial-derived metabolites, is crucial in shaping T-cell responses. Specifically, metabolites from gut microbiota (GM) exhibit robust anti-inflammatory effects, fostering the differentiation and regulation of CD8+ tissue-resident memory (TRM) cells, mucosal-associated invariant T (MAIT) cells, and stabilizing gut-resident Treg cells. Nitric oxide (NO), a pivotal
redox mediator, emerges as a central regulator of T-cell functions and gut inflammation. NO impacts the composition of the gut microbiome, driving the differentiation of pro-inflammatory Th17 cells and exacerbating intestinal inflammation, and supports Treg expansion, showcasing its dual role in immune homeostasis. This review delves into the complex interplay between GI
redox balance and GM metabolites, elucidating their profound impact on T-cell regulation. Additionally, it comprehensively emphasizes the critical role of GI
redox, particularly reactive oxygen species (ROS) and NO, in shaping T-cell phenotype and functions. These insights offer valuable perspectives on disease mechanisms and potential therapeutic strategies for conditions associated with oxidative stress. Understanding the complex cross-talk between GI
redox, GM metabolites, and T-cell responses provides valuable insights into potential therapeutic avenues for immune-mediated diseases, underscoring the significance of maintaining GI redox balance for optimal immune health.