Format

Send to

Choose Destination
Front Endocrinol (Lausanne). 2019 Jul 4;10:451. doi: 10.3389/fendo.2019.00451. eCollection 2019.

Type 2 Diabetes: How Much of an Autoimmune Disease?

Author information

1
IRCCS MultiMedica, Milan, Italy.
2
Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.
3
Unità di NeuroImmunologia, Fondazione Santa Lucia, Rome, Italy.
4
Dipartimento di Senologia, Oncologia Medica, IRCCS-Fondazione G. Pascale, Naples, Italy.
5
Dipartimento di Scienze Mediche Traslazionali, Università Degli Studi di Napoli "Federico II", Naples, Italy.
6
Treg Cell Laboratory, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Degli Studi di Napoli "Federico II", Naples, Italy.
7
Dipartimento di Biologia, Università Degli Studi di Napoli "Federico II", Naples, Italy.
8
Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
9
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain.
10
Dipartimento di Medicina e Chirurgia, Università di Salerno, Baronissi, Italy.

Abstract

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.

KEYWORDS:

T cells; autoimmunity; diabetes; immunometabolism; inflammation

Supplemental Content

Full text links

Icon for Frontiers Media SA Icon for PubMed Central
Loading ...
Support Center