期刊
FRONTIERS IN ENDOCRINOLOGY
卷 10, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fendo.2019.00451
关键词
diabetes; autoimmunity; immunometabolism; inflammation; T cells
资金
- Juvenile Diabetes Research Foundation (JDRF) [1-SRA-2018-477-S-B, 2-SRA-2018-479-S-B]
- National Multiple Sclerosis Society (NMSS) [PP-1804-30725, PP-1606-24687]
- Fondazione Italiana Sclerosi Multipla (FISM) [2016/R/10, 2016/R/18, 2018/R/4]
- Universita degli Studi di Napoli Federico II (STAR Program Linea 1 - 2018)
- Ministero della Salute [GR-2016-02363725]
- European Research Council Grant (ERC menTORingTregs) [310496]
- Telethon [GGP 17086]
- Italian Ministry of Health (Ricerca Corrente)
Type 2 diabetes (T2D) is characterized by a progressive status of chronic, low-grade inflammation (LGI) that accompanies the whole trajectory of the disease, from its inception to complication development. Accumulating evidence is disclosing a long list of possible triggers of inflammatory responses, many of which are promoted by unhealthy lifestyle choices and advanced age. Diabetic patients show an altered number and function of immune cells, of both innate and acquired immunity. Reactive autoantibodies against islet antigens can be detected in a subpopulation of patients, while emerging data are also suggesting an altered function of specific T lymphocyte populations, including T regulatory (Treg) cells. These observations led to the hypothesis that part of the inflammatory response mounting in T2D is attributable to an autoimmune phenomenon. Here, we review recent data supporting this framework, with a specific focus on both tissue resident and circulating Treg populations. We also propose that selective interception (or expansion) of T cell subsets could be an alternative avenue to dampen inappropriate inflammatory responses without compromising immune responses.
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