Role of T Lymphocytes in Type 2 Diabetes and Diabetes-Associated Inflammation.

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diabetes mellitus 1 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases
obesity 19 endocrinologydiseases

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diabetes mellitus 1201 several potential strategies that could provide successful therapies in the future.1. IntroductionType 2 diabetes mellitus (T2DM) is characterized by impaired insulin secretion, glucose intolerance, and hyperglycemia. T2DM
glucose intolerance 1274 future.1. IntroductionType 2 diabetes mellitus (T2DM) is characterized by impaired insulin secretion, glucose intolerance , and hyperglycemia. T2DM is widely viewed as a chronic, low-grade inflammatory disease caused by long-term
hyperglycemia 1299 2 diabetes mellitus (T2DM) is characterized by impaired insulin secretion, glucose intolerance, and hyperglycemia . T2DM is widely viewed as a chronic, low-grade inflammatory disease caused by long-term immune system
hypoglycemia 18804 anti-inflammatory macrophage differentiation, and reversal of glucose and insulin sensitivity without hypoglycemia [[72], [73]]. The majority of findings suggest that iNKT cells in AT play a critical role in regulating
metabolic syndrome 1426 widely viewed as a chronic, low-grade inflammatory disease caused by long-term immune system imbalance, metabolic syndrome , or nutrient excess associated with obesity [[1], [2]]. In addition, T2DM associated complications in
metabolic syndrome 14083 CD8+ Cytotoxic T CellsThe inflammation of adipose tissue is considered as a key event leading to the metabolic syndrome , diabetes, and atherosclerotic cardiovascular disease. It was reported that, within two weeks of high-fat
obesity 1481 caused by long-term immune system imbalance, metabolic syndrome, or nutrient excess associated with obesity [[1], [2]]. In addition, T2DM associated complications in the kidneys, arteries, and eyes are also manifested
obesity 1916 Hotamisligil et al. reported an increase of TNF-α in adipose tissue from different animal models of obesity and diabetes. Neutralization of TNF-α in obese rats improved peripheral glucose uptake [[4]]. Studies
obesity 2125 Studies have indicated that other inflammatory cytokines such as IL-1β and IFN-γ which are increased in obesity and diabetes also modulate insulin signaling [[5], [6]]. On the other hand, a number of anti-inflammatory
obesity 3293 inflammation.2. Th1 and Th2 CellsIncreasing evidence suggests a pathological role for CD4+ T cells in obesity and insulin resistance. Obesity is a major critical risk factor for T2DM. A recent study by Shirakawa
obesity 3658 and CD153 and displayed characteristics of cellular senescence [[10]]. It has also been shown that obesity induces MHC class II expression on adipocytes and thus activates CD4+ T cells to initiate adipose tissue
obesity 3857 adipose tissue inflammation [[11]]. These studies suggest CD4+ T cells may play an important role in obesity and obesity-induced insulin resistance.CD4+ effector T cells can be further divided into proinflammatory
obesity 3869 tissue inflammation [[11]]. These studies suggest CD4+ T cells may play an important role in obesity and obesity -induced insulin resistance.CD4+ effector T cells can be further divided into proinflammatory Th1, Th17,
obesity 5098 liver, muscle, and pancreas. Macrophages are the major inflammatory cells in the adipose tissue in obesity , increasing from 5–10% in lean subjects to up to 50% in obese individuals [[8], [9]]. Based on their
obesity 6135 anti-inflammatory IL-4 and IL-13 to skew the differentiation of macrophage towards M2 [[19], [20]]. In diet-induced obesity , CD4+T cells were increased in the adipose tissue and induced the recruitment and differentiation of
obesity 6494 of proinflammatory M1 versus anti-inflammatory M2 was viewed as a key factor in the development of obesity and T2DM [[17]]. Therefore, Th1 and Th2 responses, which are closely related to M1/M2 polarization,
obesity 6635 and Th2 responses, which are closely related to M1/M2 polarization, may also have a critical role in obesity and T2DM.Several clinical studies have confirmed that Th1 was upregulated in the adipose tissue and
obesity 9191 shown that IL-17 could stimulate the production of TNF-α, the first cytokine being associated with obesity and insulin resistance. It is reported that intestinal Th17 cells may induce AMPs, specifically Reg3b
obesity 10079 have not yet been identified in AT from lean or obese animals [[38]]. Whether CD103 DCs can regulate obesity -induced inflammation in AT by influencing the balance of Treg and Th17 cell differentiation in vivo
obesity 13427 associated with the stability and the suppressive function of Foxp3+Treg cells. T2DM patients with obesity showed a significantly lower level of CD39hi Treg compared with overweight controls [[51]]. It was reported
obesity 17309 differentiation 45RA (CD45RA+) cells, indicating γδ T cells are also involved in inflammation in obesity and diabetes [[62]]. A recent study reported that IL-2 treatment rescued Vγ9Vδ2 T cell cytokine production
obesity 18250 regulatory role in congenic parabiotic mice [[69]]. However, adipose iNKT cells are obviously decreased in obesity [[65], [66], [70]]. iNKT cells can regulate the cross talk between innate and adaptive immunity as potent
obesity 18630 (αGalCer), a potent lipid ligand, could activate iNKT cell. It is shown that injection of αGalCer in obesity increases the iNKT cell amount and induces weight loss rapidly, anti-inflammatory macrophage differentiation,
obesity 18985 play a critical role in regulating local inflammation and protecting against metabolic disorder in obesity [[74]].8. ConclusionIn conclusion, there is increasing evidence linking the activation of T lymphocytes
obesity 19323 autoimmune disease [[75]]. Understanding the role of specific immune cells and proinflammatory molecules in obesity and diabetes is required for developing novel therapeutic approaches to modulate metabolic inflammation

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