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The Alterations in and the Role of the Th17/Treg Balance in Metabolic Diseases

期刊

FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.678355

关键词

Th17; Treg; chronic inflammation; metabolic disease; obesity; T2DM; MAFLD

资金

  1. Engineering Technology Research Center for Personalized Precision Diagnosis and Treatment, Science and Technology Department of Jilin Province [20170623005TC]
  2. Innovation Capability Project of Jilin Provincial Development and Reform Commission [2017C019]
  3. Department of Science and Technology of Jilin Province [20190701040GH]

向作者/读者索取更多资源

Chronic inflammation is crucial in the development of metabolic diseases, with the Th17/Treg balance being regulated by inflammatory cytokines and metabolic factors, potentially through metabolism-related signaling pathways and epigenetic regulation.
Chronic inflammation plays an important role in the development of metabolic diseases. These include obesity, type 2 diabetes mellitus, and metabolic dysfunction-associated fatty liver disease. The proinflammatory environment maintained by the innate immunity, including macrophages and related cytokines, can be influenced by adaptive immunity. The function of T helper 17 (Th17) and regulatory T (Treg) cells in this process has attracted attention. The Th17/Treg balance is regulated by inflammatory cytokines and various metabolic factors, including those associated with cellular energy metabolism. The possible underlying mechanisms include metabolism-related signaling pathways and epigenetic regulation. Several studies conducted on human and animal models have shown marked differences in and the important roles of Th17/Treg in chronic inflammation associated with obesity and metabolic diseases. Moreover, Th17/Treg seems to be a bridge linking the gut microbiota to host metabolic disorders. In this review, we have provided an overview of the alterations in and the functions of the Th17/Treg balance in metabolic diseases and its role in regulating immune response-related glucose and lipid metabolism.

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