Suppr超能文献

微生物组激活与适应性免疫调节。

Microbiota activation and regulation of adaptive immunity.

机构信息

Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Department of Oncology, Western University, London, ON, Canada.

出版信息

Front Immunol. 2024 Oct 9;15:1429436. doi: 10.3389/fimmu.2024.1429436. eCollection 2024.

Abstract

In the mucosa, T cells and B cells of the immune system are essential for maintaining immune homeostasis by suppressing reactions to harmless antigens and upholding the integrity of intestinal mucosal barrier functions. Host immunity and homeostasis are regulated by metabolites produced by the gut microbiota, which has developed through the long-term coevolution of the host and the gut biome. This is achieved by the immunological system's tolerance for symbiote microbiota, and its ability to generate a proinflammatory response against invasive organisms. The imbalance of the intestinal immune system with commensal organisms is causing a disturbance in the homeostasis of the gut microbiome. The lack of balance results in microbiota dysbiosis, the weakened integrity of the gut barrier, and the development of inflammatory immune reactions toward symbiotic organisms. Researchers may uncover potential therapeutic targets for preventing or regulating inflammatory diseases by understanding the interactions between adaptive immunity and the microbiota. This discussion will explore the connection between adaptive immunity and microbiota.

摘要

在黏膜中,免疫系统的 T 细胞和 B 细胞通过抑制对无害抗原的反应和维持肠道黏膜屏障功能的完整性,对维持免疫稳态至关重要。宿主免疫和稳态受肠道微生物群产生的代谢物调节,这些代谢物是通过宿主和肠道生物群落的长期共同进化而产生的。这是通过免疫系统对共生微生物群的耐受性以及对侵袭性生物产生促炎反应的能力来实现的。与共生生物体的肠道免疫系统失衡导致肠道微生物组的稳态紊乱。这种失衡导致微生物群落失调、肠道屏障完整性减弱以及对共生生物体的炎症免疫反应的发展。通过了解适应性免疫与微生物组之间的相互作用,研究人员可能会发现预防或调节炎症性疾病的潜在治疗靶点。本讨论将探讨适应性免疫与微生物组之间的联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073b/11496076/e47c340ebb5a/fimmu-15-1429436-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验