Role of Adaptive and Innate Immunity in Type 2 Diabetes Mellitus

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diabetic retinopathy 1 endocrinologydiseases
glucose intolerance 4 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
obesity 22 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
diabetes mellitus 2 endocrinologydiseases

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diabetes mellitus 652 11/2018AbstractAfter the recognition of the essential role of the immune system in the progression of type 2 diabetes mellitus , more studies are focused on the effects produced by the abnormal differentiation of components of the
diabetes mellitus 1612 roles, aiming to provide new thought for the development of immunotherapy in T2DM.1. IntroductionType 2 diabetes mellitus (T2DM) is characterized by abnormally elevated levels of blood glucose due to impaired insulin secretion,
diabetic retinopathy 7581 HbA1c variance [[28]]. During the progression of T2DM, levels of mRNA and protein of IL-2 and TNF-α in diabetic retinopathy (DR) patients were dramatically higher compared with those of the healthy control group [[29]]. Moreover,
glucose intolerance 1736 is characterized by abnormally elevated levels of blood glucose due to impaired insulin secretion, glucose intolerance , and hyperglycemia. It is also considered as a major burden for healthcare systems worldwide [[1]].
glucose intolerance 13620 NKT cells enhances the presence of M1 macrophages in visceral AT and increases insulin resistance and glucose intolerance [[63]]. It was reported that there was decreased frequency of iNKT cells in VAT and peripheral blood
glucose intolerance 15922 These results indicated that B cells participated in the process of promoting insulin resistance and glucose intolerance by activating Th1 and Th17 cells and releasing pathogenic antibodies.4. NK Cells in T2DMNK cells could
glucose intolerance 19589 macrophage), thereby playing a key role in the development of diet-induced obesity, insulin resistance, and glucose intolerance .Furthermore, macrophage activation is mediated by cells involved in adaptive immunity. Th1 and Th17
hyperglycemia 1761 abnormally elevated levels of blood glucose due to impaired insulin secretion, glucose intolerance, and hyperglycemia . It is also considered as a major burden for healthcare systems worldwide [[1]]. Nowadays, the pathogenesis
obesity 815 produced by the abnormal differentiation of components of the immune system. In patients suffering from obesity or T2DM, there were alterations in proliferation of T cells and macrophages, and impairment in function
obesity 2176 mechanisms controlling immune cell lineage determination, function, and migration are implicated in obesity and T2DM. Obesity is associated with low-grade inflammation and is responsible for the activation of
obesity 2470 patients can induce metabolic dysregulation. It has also been recognized that insulin resistance during obesity is closely related to adipose tissue inflammation [[4]]. The abnormal proliferation of factors of innate
obesity 4016 differentiated in T2DM patients.2.1. CD4+ T CellsCD4+ T cells play an important role in the pathology of obesity and insulin resistance. CD4+ effector T cells can be further subdivided into proinflammatory Th1 and
obesity 6679 (TNF-) α, IFN-γ, and IL-17) and T lymphocytes was drastically upregulated during the pathogenesis of obesity -induced insulin resistance and development of T2DM [[23]–[25]]. With respect to the relationship between
obesity 9983 decreased in patients suffering from T2DM [[44]]. High levels of insulin in a model of diet-induced obesity impaired the ability of Tregs to suppress inflammatory responses via the AKT/mTOR signaling pathway,
obesity 12003 when compared with lean individuals, which might modulate the insulin resistance [[56]]. Diet-induced obesity did not affect the maintenance of preexisting memory CD8+ T cells, including acquisition of a long-term
obesity 12792 can secrete high levels of cytokines, including IL-4 and IFN-γ. But as adipose tissue expands during obesity , the number of iNKT cells decreased, correlating with proinflammatory macrophage infiltration. Mice
obesity 14940 HFD induced a significant increase in the proliferation of B cells in VAT [[70]]. In patients with obesity or T2DM, DNA methylation, which is likely to be an important mechanism contributing to the interindividual
obesity 17958 differentiation into a proinflammatory M1 phenotype which further promotes inflammation and the development of obesity -induced insulin resistance [[81]].5. Myeloid Cells in T2DMInnate immunity also includes macrophages,
obesity 18198 eosinophils, and basophils. Macrophages were emphasized to play a key role in the pathological progress of obesity or insulin resistance. Two subtypes of macrophages are present in the adipose tissue: a proinflammatory
obesity 18799 IL-10 [[82]]. Macrophages infiltrated into expanding adipose tissue causing inflammation and linking obesity to insulin resistance. In obese humans, AT macrophages displayed profound proinflammatory (M1) polarization,
obesity 19556 macrophage activation (M2-like macrophage), thereby playing a key role in the development of diet-induced obesity , insulin resistance, and glucose intolerance.Furthermore, macrophage activation is mediated by cells
obesity 20613 specifically upregulated in adipose tissue macrophages (ATMs), particularly in CD11c+ M1 ATMs, due to obesity , which could further promote expression of proinflammatory cytokines by enhancing activity of nuclear
obesity 20875 cells (NK-κB) [[89]].Beside altered macrophages, monocytes also play a key role in the progression of obesity and insulin resistance in T2DM patients. Patients suffering from T2DM exhibited increased expression
obesity 23977 diabetic mice [[98]].7. ConclusionSince there were many similarities in the pathological progress of obesity and T2DM, which are tightly linked, altered proliferation, function, or infiltration of components of
obesity 24583 protective NK cells. A higher susceptibility to infections has been observed in patients suffering from obesity and T2D, which indicates a T cell homeostatic dysregulation, NK cell dysfunction, and abnormal polarization
obesity 24775 and abnormal polarization of macrophages (Figure 1). Metabolic alterations in patients suffering from obesity and T2DM may further affect differentiation, function, and survival of components of innate immunity
obesity 25396 suffering from type 2 diabetes are still not completely understood. The signals and mechanisms involved in obesity - and/or T2D-mediated modulation of T cell functions remain poorly documented. The mechanisms explaining
obesity 26053 autoimmune disease because of the importance of inflammation in the development of insulin resistance, obesity , and T2DM. It is necessary to understand the role of innate immunity and adaptive immunity in obesity
obesity 26155 obesity, and T2DM. It is necessary to understand the role of innate immunity and adaptive immunity in obesity and diabetes, which could reveal novel immunotherapeutic approaches to modulate metabolic inflammation
obesity 26369 insulin resistance.Figure 1Role of innate immunity and adaptive immunity in the condition of T2DM, obesity , or adipose tissue of HFD mice
type 2 diabetes mellitus 645 11/2018AbstractAfter the recognition of the essential role of the immune system in the progression of type 2 diabetes mellitus , more studies are focused on the effects produced by the abnormal differentiation of components of the

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