Abstract
Type 1 diabetes (T1D) and type 2 diabetes (T2D) are multifactorial diseases with different etiologies in which chronic inflammation takes place. Defects in invariant natural killer T (iNKT) cell populations have been reported in both T1D and T2D patients, mouse models and our recent study revealed mucosal-associated invariant T (MAIT) cell defects in T2D and obese patients. Regarding iNKT cells many studies in non-obese diabetic mice demonstrated their protective role against T1D whereas their potential role in human T1D is still under debate. Studies in mouse models and patients suggest that iNKT cells present in adipose tissue (AT) could exert a regulatory role against obesity and associated metabolic disorders, such as T2D. Scarce data are yet available on MAIT cells; however, we recently described MAIT cell abnormalities in the blood and ATs from obese and T2D patients. These data show that a link between MAIT cells and metabolic disorders pave the way for further investigations on MAIT cells in T1D and T2D in humans and mouse models. Furthermore, we hypothesize that the gut microbiota alterations associated with T1D and T2D could modulate iNKT and MAIT cell frequency and functions. The potential role of iNKT and MAIT cells in the regulation of metabolic pathways and their cross-talk with microbiota represent exciting new lines of research.
Highlights
According to the WHO diabetes will be in 2030 the seventh leading cause of death [1]
INKT cells exert a regulatory role in Type 1 diabetes (T1D), while their role in Type 2 diabetes (T2D) is still matter of debate
We showed that iNKT17 cells infiltrate the pancreas of non-obese diabetic (NOD) mice and promote diabetes development. α-GalCer treatment suppresses IL-17 produced by Invariant natural killer T (iNKT) cells, which could contribute to the protective role of α-GalCer in T1D [16]
Summary
According to the WHO diabetes will be in 2030 the seventh leading cause of death [1]. Numerical and functional iNKT cell defects in NOD mice have been identified: reduced iNKT cell frequency and IL-4 production [8, 9]. The first data obtained in patients with T1D showed a decreased frequency of iNKT cells as well as a defect in IL-4 production [32] but since, contradictory results from clinical studies have been published; some following reports have supported this finding [33, 34], while one report has shown increased numbers of iNKT cells [35], and others did not find differences in iNKT cell numbers [36,37,38,39].
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