TY - JOUR
T1 - Type 2 Diabetes
T2 - How Much of an Autoimmune Disease?
AU - de Candia, Paola
AU - Prattichizzo, Francesco
AU - Garavelli, Silvia
AU - De Rosa, Veronica
AU - Galgani, Mario
AU - Di Rella, Francesca
AU - Spagnuolo, Maria Immacolata
AU - Colamatteo, Alessandra
AU - Fusco, Clorinda
AU - Micillo, Teresa
AU - Bruzzaniti, Sara
AU - Ceriello, Antonio
AU - Puca, Annibale A
AU - Matarese, Giuseppe
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
U2 - 10.3389/fendo.2019.00451
DO - 10.3389/fendo.2019.00451
M3 - Article
C2 - 31333589
VL - 10
SP - 451
JO - Frontiers in Endocrinology
JF - Frontiers in Endocrinology
SN - 1664-2392
ER -