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reverses diabetes type 2 untreated (πŸ”₯ statistics) | reverses diabetes type 2 naturehow to reverses diabetes type 2 for Front Endocrinol (Lausanne). 2019; 10: 451.
Published online 2019 Jul 4. doi:Β 10.3389/fendo.2019.00451
PMCID: PMC6620611
PMID: 31333589

Paola de Candia

1IRCCS for 1 last update 03 Jul 2020 MultiMedica, Milan, Italy1IRCCS MultiMedica, Milan, Italy

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Francesco Prattichizzo

1IRCCS MultiMedica, Milan, Italy

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Silvia Garavelli

reverses diabetes type 2 food list (⭐️ food choices) | reverses diabetes type 2 rangehow to reverses diabetes type 2 for 2Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy

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Veronica De Rosa

2Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy

3Unità di NeuroImmunologia, Fondazione Santa Lucia, Rome, Italy

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Mario Galgani

2Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy

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Francesca Di Rella

4Dipartimento di Senologia, Oncologia Medica, IRCCS-Fondazione G. Pascale, Naples, Italy

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Maria Immacolata Spagnuolo

5Dipartimento di for 1 last update 03 Jul 2020 Scienze Mediche Traslazionali, Università Degli Studi di Napoli “Federico II”, Naples, Italy5Dipartimento di Scienze Mediche Traslazionali, Università Degli Studi di Napoli “Federico II”, Naples, Italy

Alessandra Colamatteo

6Treg Cell Laboratory, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Degli Studi di Napoli “Federico II”, Naples, Italy

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Clorinda Fusco

6Treg Cell Laboratory, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Degli Studi di Napoli “Federico II”, Naples, Italy

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Teresa Micillo

7Dipartimento di Biologia, Università Degli Studi di Napoli “Federico II”, Naples, Italy

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2Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy

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8Institut for 1 last update 03 Jul 2020 D''Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain8Institut D''Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

9Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain
10Dipartimento di Medicina e Chirurgia, Università di Salerno, Baronissi, Italy
Edited by: Oreste Gualillo, Servicio Gallego de Salud, Spain
Reviewed by: Morena Scotece, Instituto de Investigación Biomédica de A Coruña (INIBIC), Spain; Eloi Franco-Trepat, Health Research Institute of Santiago of Compostela (IDIS), Spain
*Correspondence: Paola de Candia [email protected]
Giuseppe Matarese [email protected]
This article was submitted to Translational Endocrinology, a section of the journal Frontiers in Endocrinology
Received 2019 Apr 12; Accepted 2019 Jun 21.
Copyright © 2019 de Candia, Prattichizzo, Garavelli, De Rosa, Galgani, Di Rella, Spagnuolo, Colamatteo, Fusco, Micillo, Bruzzaniti, Ceriello, Puca and Matarese.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Associated Data

Data Availability Statement

No datasets were generated or analyzed for this study.

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: diabetes, autoimmunity, immunometabolism, inflammation, T cells

Introduction

Type 2 diabetes (T2D) is a multifactorial and multilayer disease, characterized by an altered metabolism of glucose, fat and proteins. Hyperglycemia is the main common feature defining T2D, and clusters of patients are identifiable according to the specific combination of insulin resistance (IR) and absolute or relative insulin deficiency (1), a combination that leads to complex clinical trajectories underlying the development of early metabolic imbalances and later cardiovascular complications (2, 3). T2D and its complications remain major causes of morbidity and mortality in the western world (4).

While it is well established that type 1 diabetes (T1D) results from cell-mediated autoimmune pancreatic β cell destruction, T2D has been historically considered a metabolic disease, and metabolic determinants are traditionally identified as major pathogenetic factors. A more recent line of research has started to focus on low-grade inflammation (LGI) as a pervasive feature of T2D, accompanying the development and the progression of the disease, as well as the genesis of complications (5). Two of the main risk factors to develop T2D are aging and obesity, both known to promote tissue and systemic chronic inflammation, often referred to as inflammaging and metaflammation, respectively (58). A number of publications demonstrate that inflammation is not a mere bystander but it plays a key role in the progression of all the main features of T2D disease, e.g., IR, β cell failure or inability to cope with increased insulin demand, and atherosclerotic plaque development and destabilization (57). A plethora of putative inflammatory sources and mechanisms have been proposed to explain this evidence (59). Seminal discoveries and the majority of studies have mainly focused on cells of the innate immune system (1012) and more recent data also suggest the direct involvement of acquired immunity. In particular, autoimmunity, a multifactorial process defined by loss of self-tolerance and chronic excess reactivity of B and T cells, has started to be recognized as an overlapping mark of both T1D and T2D. Furthermore, metabolic dysregulation and autoimmune components are able to generate a vicious cycle: the increased production of cytokines characterizing the chronic inflammatory state in T2D concur to destroy pancreatic β cells, and this inflammation-induced tissue damage leads to the release of “self” antigens that promote autoimmune activation. In turn autoimmunity further impairs insulin secretion in β cells and promotes hyperglycaemia (1315).

A better recognition of the autoimmune components of T2D is relevant because it may lead to a deeper understanding of the mechanisms involved in the insurgence of hyperglycemia; it has also considerable therapeutic consequences, translating into a better classification and treatment of the disease. Indeed, T2D patients with a significant autoimmune component: (i) need insulin earlier during disease progression, (ii) are likely to poorly respond to classical anti-diabetic medications, (iii) may be highly responsive to immunomodulator therapy (16).

Our review focuses on existing evidence on autoimmune aspects of T2D from a molecular, cellular and clinical perspective. We describe how the knowledge regarding the intimate link between metabolism and inflammatory responses in specific immune cell populations is rapidly expanding, and report latest findings regarding the alteration of B and T (with a specific focus on T regulatory subsets) cells, the metabolic mechanisms driving their expansion or dysfunction in T2D (1720). Finally, we briefly summarize promising clinical data regarding the potential of anti-inflammatory therapies in T2D and hypothesize a framework where inflammatory responses are modulated, rather than suppressed, to intercept and blunt the development and progression of the disease.

Latent Autoimmune Diabetes of the Adult (LADA)

The presence of circulating autoantibodies in non-insulin-dependent diabetes mellitus was first identified more than 40 years ago (21). Nowadays, the presence of these autoantibodies characterizes a condition referred to as latent autoimmune diabetes of the adults (LADA). Autoantibodies against glutamic acid decarboxylase (GADA), islet cytoplasm (ICA), insulinoma-associated protein (IA-2A), and zinc transporter (ZnT8A) are commonly found in these patients.

Analyzing a large cohort of T2D patients (n = 3.672) from the UK, aged between 25 and 65 years, the percentage of subjects with ICA and/or GADA autoantibodies was found to be 12% overall and to be significantly higher in younger patients (22). Another study from the Pittsburgh cohort of the Cardiovascular Health Study found that also among diabetic patients aged over 65 years 12% had autoantibodies against GAD65 and/or IA-2, associated with an abnormal glucose control and a pronounced activation of the acute-phase response (increased fibrinogen and C-reactive protein levels), that may in part explain the observed defect in insulin secretion (23). A similar prevalence of diabetes autoimmunity was described in Argentinian elderly T2D patients (24). The largest European study (Action LADA) to date has later analyzed 6,156 T2D patients (age range, 30–70 years) for GADA, IA-2A and ZnT8A and found that 9.7% were positive, with the majority (8.8%) being GADA positive, and that, at diagnosis, these patients are usually non-insulin requiring and do not show categorically distinct clinical features from autoantibody-negative T2D patients (25). Ethnicity may count, as GADA positivity in T2D patients range from 3.8% in Japan (Eihme Study, n = 4,980) (26) to 10% in Norway (HUNT Study, n = 1,134) (27).

At diagnosis, LADA patients do not usually need exogenous insulin and they appear to be clinically affected by T2D, but a large percentage will need it within a few years, showing a much faster decline of β cell function compared to T2D patients, possibly caused by the ongoing immune-mediated β cell destruction. Notably, Turner et al. showed that 94% of patients with ICA and 84% of those with GADA required insulin therapy by 6 years, compared with 14% of those without the antibodies (22). A small study has directly correlated the presence of islet autoantibodies with significantly lower acute insulin response when compared to that of the autoantibody-negative group, but observed similar peripheral IR, providing compelling evidence that the profound impairment of insulin secretion is plausibly determined by the immune-mediated injury of pancreatic β cells (28).

LADA at the Intersection of Type 1 and Type 2 Diabetes

Although formally classified as T1D for the typical presence of autoantibodies, LADA patients present several clinical features that are mixed between T1D and T2D pathologies. Low birthweight results to be a risk factor for LADA of the same strength as for T2D, suggesting LADA etiology includes factors related to T2D (29). Furthermore, LADA is associated with factors well known to promote T2D, such as overweight, physical inactivity, smoking, and sweetened beverage intake, suggesting LADA may in part be preventable through the same lifestyle modifications as T2D (30). In particular, the risk of LADA in relation to overweight/obesity was studied in two large population-based reports from a Swedish case-control study and the Norwegian HUNT Study, whose findings support the hypothesis that, even in the presence of autoimmunity, factors linked to IR, such as excessive weight, could promote LADA onset (31). Metabolomics of LADA, T1D and T2D patients failed to identify a unique metabolite profile for any of the diabetes types. Instead, the metabolome varied along a C-peptide-driven continuum from T1D to T2D, with LADA being an intermediate and patients metabolically closer to T1D showing a faster progression to insulin therapy than those closer to T2D (32). On the other hand, a Danish study analyzing a cohort of 4,374 adults with newly diagnosed diabetes demonstrated that fasting C-peptide and GADA status, but not age at onset, are able to define groups of diabetic patients with clinically relevant differences in glycaemic control and cardiometabolic risk, suggesting that the borders between T1D and LADA may be less discrete than believed (33). Parallel studies also demonstrated that LADA is associated with lower prevalence of microvascular complications, lower mortality, and lower risk of cardiovascular events, compared with T2D (34, 35). The risk of LADA is substantially increased with family history of T1D disease but also, albeit significantly less so, of T2D disease (36). A meta-analysis from 16 independent case-control studies (8,869 cases and 20,829 controls total), aimed at determining the association of T1D and T2D gene variants, demonstrated that some of these polymorphisms are associated with the risk of LADA, further supporting the idea of LADA as a combination of both T1D and T2D and emphasizing its heterogeneity (37). The first genome-wide association study of LADA revealed how the leading genetic signals were principally shared with T1D, although positive genetic correlations genome-wide were registered also with T2D. Authors identified a novel independent signal at the known T1D locus harboring the 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3 (PFKFB3) gene (38). This gene encodes a regulator of glycolysis and insulin signaling and thus it had been previously reported as a plausible biological candidate in T2D diabetes (39). PFKFB3 also causes a reduction in T cell glucose consumption and survival, which in turn impairs the immune response in autoimmune conditions (40), calling for further studies to determine whether this genetic factor is truly a distinguishing feature between adult and childhood-onset autoimmune diabetes (38).

To further complicate the picture, while subjects classified as T2D patients are by definition autoantibody negative, autoantibodies may however also fluctuate. The Norwegian HUNT study unveiled that about 3% of subjects classified as T2D show a transient autoantibody positivity associated with earlier disease onset, a pre-diagnostic evidence of autoimmune activity in a sub-group of T2D patients (41).

LADA patients tend to share some clinical and phenotypic characteristics, compared to autoantibody-negative T2D patients: they are usually younger and leaner, suffer from acute symptoms and have a personal and/or familial history of autoimmune diseases (25). Nevertheless, LADA heterogeneity (from patients with clear signs of insulin deficiency associated with strong markers of autoimmunity, to patients showing weak markers of autoimmunity and closely resembling T2D) is possibly the mirror of a progressive and continuous clinical spectrum that blends, instead of discriminating, T1D and T2D (Figure 1). The crucial question arises: how important is the autoimmune component in autoantibody negative T2D patients? To try and answer to this question, we cannot abstain from describing the connection that exists between systemic metabolism and the immune system.

The continuous range of diabetes. Notwithstanding the different risk factors, instead of being clearly confined, T1D, LADA, and T2D patients are now known to present overlaying/overlapping clinical characteristics. LADA patients range from showing clear signs of β cell dysfunction (insulin deficiency and low levels of C-peptide) associated with strong markers of autoimmunity (presence of islet-cell autoantibodies) to patients showing a higher grade of insulin resistance and other pathological components resembling T2D condition [metabolic syndrome and systemic low-grade inflammation (LGI)]. The pathological features of the different forms of diabetes manifest as an uninterrupted spectrum that fails to clearly discriminate T1D and T2D.

The Immune-Metabolic Connection

Obesity, together with age, is the major risk factor for T2D. A large proportion of T2D patients are obese and the risk of T2D increases with increasing body mass index (BMI) (42). In both human and mice, obesity is associated with chronic LGI, thought to play a pivotal role in the development of IR and T2D pathological process (14). Although obesity is not yet a fully established risk factor for autoimmunity, the altered glucose tolerance and the development of IR due to an abnormal accumulation of adipose tissue (AT) in obese subjects coincide with an elevated incidence of autoimmune diseases (43). Epidemiological data analyzing T1D, multiple sclerosis, and psoriasis patients have recognized a causal risk factor for all these autoimmune conditions in an elevated BMI (4446), although the mechanistic players of this association remain mostly undetermined. The coexistence of overweight and autoimmunity may be the result of concurrent dysregulation of immune tolerance, involving different organs (47). In the case of T2D, one of the most implicated districts is the AT (48).

The presence of enlarged fat depots that characterizes overweight/obese subjects, may be considered as an autoimmune pathology in which autoreactive T cells attack the adipocytes and fuel adipose inflammation (49, 50). On the other hand, AT is actually contiguous with main immune cell centers, such as lymph nodes, thymus, and bone marrow, in a close embrace that we have recently defined an “anatomical tango” (51). AT surrounds the thymus, hence may influence T cell differentiation in response to metabolic cues (52); furthermore, a high number of adipocytes resides in the bone marrow, with possible involvement in haematopoiesis, lymphopoiesis, and memory B and T cell responses (53). This physical contiguity has been noted by anatomists of the past, but only recently, though, it has been explored from a new and mechanistic point of view, and researchers have hypothesized and tested how it may allow a continuous communication (51).

The AT produces and releases several bioactive molecules, referred to as adipokines with a variety of pro-inflammatory and anti-inflammatory roles, which regulate both metabolism and immune cell function (20). Together with immune-cell derived cytokines, these immune metabolic mediators actually allow a reciprocal regulation between the AT and the immune system at both a paracrine and endocrine level (54, 55). One of the most biologically relevant of these molecules, leptin, is produced by the AT in proportion to the body fat mass and, at a systemic level, regulates appetite and food intake, promoting the entry of glucose into the tissues and reducing hyperglycemia (56). Leptin links lifestyle with inflammatory and/or autoimmune molecular mechanisms (5759). It is not only known to significantly regulate the innate immune cells, but to also bridge obesity and dysregulated adaptive T cell activity. It seems that metabolic dysregulation both induces and depends on autoimmune alterations (60, 61). As a double edge sword, lymphocyte activation and function are intimately intertwined between metabolic disorders, including T2D, and inflammatory diseases (62, 63).

The research at the interface between the historically distinct disciplines of immunology and metabolism (immunometabolism) focuses on the regulatory connection between the metabolic state of an organism and immune cell physiology/activity. Unveiling this connection is endowed with enormous potential for T2D understanding (64).

While the involvement of AT-resident macrophages and innate immunity has been thoroughly analyzed (65, 66), fewer studies have focused on the role played by the adaptive immune B and T lymphocytes and their released factors in obesity-associated inflammation and T2D triggering events. Next, we critically review these studies.

B Cell Alteration in T2D

B lymphocytes are responsible for the humoral immunity component of the adaptive immune system. Beyond antibody secretion, they can also present antigens and secrete cytokines. A plethora of B cell subsets have been identified according to the stage of differentiation, tissue localization and developmental lineage (67). Despite the controversies regarding the correspondence between human and murine B cells (68, 69), different alterations affecting both circulating and tissue-resident B cells have been described in T2D (70). Similarly, both antibody-mediated and contact-dependent mechanisms have been proposed in relation to B cell imbalance and loss of insulin sensitivity.

A clear demonstration supporting the role of B cells also in the development of IR has been provided in murine models. B cell–null New Zealand obese mice do not develop IR in response to obesity (71). Similarly, another study showed that either pharmacological or genetic depletion of B cells is sufficient to significantly attenuate immune cell infiltration and inflammation in the AT, finally promoting insulin sensitivity (72). Mechanistically, high fat diet (HFD) has been proposed to foster the early recruitment of B cells which promote T cell activation in the AT. In turn, this would boost M1 macrophage polarization, and thus induce IR. B cells can also exert detrimental effects systemically through the production of pathogenic IgG antibodies (73). Treatment of B cell-null mice with IgGs derived from WT mice exposed to HFD is sufficient to phenocopy the metabolic alterations induced by HFD (72). In addition, recent findings revealed that hyposialylated IgGs activate endothelial IgG receptor FcγRIIB to promote obesity-induced IR. Of note, the results were replicated with IgGs derived from patients with T2D and transferred to IgG-deficient mice, suggesting the relevance of this mechanism also for human diabetes (74). Consistently, human subjects with IR are characterized by 122 potential IgG targets (72). However, the wide range of possible antigens, their relatively low prevalence, and the absence of an evident tissue lesion (in any diabetes-relevant tissue) argue against a prototypical autoimmune phenomenon for T2D. On the other hand, a similar setting is compatible with low grade inflammation, a subclinical, chronic process without major manifestations of the acute inflammatory response (5). Similar findings expanded these results showing that B-T cell contact is mandatory to develop a pathogenic pro-inflammatory response. Indeed, the addition of a cytokine-permeable trans-well membrane blunted the B cell-induced Th17 response (75). Moreover, B cells from diabetic patients showed reduced secretion of the anti-inflammatory interleukin (IL)-10 upon stimulation (75), a phenomenon observed in multiple cell types exposed to the diabetic environment (9). Regarding specific B cell subpopulations, less is known about their deregulation in T2D, especially considering human data. Naïve B cells are divided into two subsets, the most abundant B-2 follicular and marginal zone B cells, responsible for generating the majority of high-affinity antibodies during an infection and the scarcer B-1 cells, arising from a different developmental pathway and able to generate natural antibodies in a T cell-independent manner (76). AT-resident, B-2 cells were identified to promote the inflammatory response to HFD and IR, possibly through a leukotriene B4 (LTB4) - LTB4 receptor 1 axis (77). Interestingly, two studies reported a protective role for both CD5+ B-1a and CD5 B-1b cells [different at both phenotypic and development level (78)] in HFD-induced metabolic alterations in mouse models. Adoptive transfer of both B-1a and B-1b cells into HFD-fed, B cell–deficient mice ameliorated IR and glucose intolerance through IL-10 and polyclonal IgM-dependent mechanisms, while the transfer of B-2 cells worsened the metabolic imbalances (79, 80). Consistently, diabetic leptin receptor-mutant db/db mice had lower levels of peritoneal B-1a cells, which were also hypo-responsive in terms of differentiation to effector B cells and IgM production (81). On the other hand, one study reported conflicting results, since it showed that the suppression of B cell activation in AT of obese mice fail to discernibly affect systemic inflammation and glucose homeostasis (82). Findings in obese subjects demonstrate that B-1 cells and IgM antibodies in AT inversely correlate to inflammation and IR (80). Circulating populations of B cells in T2D patients further support a B-1 protective, B-2 detrimental paradigm since B-1a cell frequency are inversely correlated with HbA1c, LDL, and triglycerides, while B-2 cells show the opposite trend (83).

reverses diabetes type 2 dinner recipes (β˜‘ quick fix) | reverses diabetes type 2 visionhow to reverses diabetes type 2 for The resulting corollary to these observations is that patients with T2D may be characterized by an altered response to vaccination and a higher susceptibility to infections. B cell number and capacity to produce Ig are known to decline with age (84), while few data are available for T2D patients. Elderly patients are characterized by an altered response to vaccinations and infections, despite a higher basal pro-inflammatory status (84, 85). Similarly, B cells derived from T2D patients are characterized by a reduced ability to produce de novo antibody responses, despite a higher basal secretion of pro-inflammatory cytokines (86) but B cell repertoire appears to be affected by obesity, rather than by the diabetic status (87). Nonetheless, the incidence of a wide range of infective diseases is markedly increased in the diabetic population (88, 89). On the other hand, data regarding immune response to vaccination in T2D are not straightforward. In particular, unaltered or even optimal response to influenza vaccination has been reported in young and elderly patients with T2D (9092). Guidelines for medical care strongly recommend annual influenza vaccination for diabetic patients (93) and a recent systematic review emphasizes and reinforces the need and value of seasonal vaccination to decrease severe complications, hospitalization and/or death in diabetic patients (94). Results regarding other vaccinations are sparser (95, 96).

Overall, more observational and mechanistic data are needed to identify the involvement of B cells in the development of IR and T2D. In particular, few prospective studies have been conducted in humans. Reported alterations in T2D patients could represent either a cause or a consequence of the disease. Nonetheless, the observations that (i) specific antibodies are associated with prevalent T2D (97); (ii) serum IgG2 levels are associated with whole-body insulin-mediated glucose disposal (98); and (iii) general abundance of circulating gamma globulins predicts incident T2D in a large cohort (99), support the postulate that B cell alteration plays a key role in T2D pathogenesis.

CD4+CD25high T Regulatory Cells, Masters of Tolerance

reverses diabetes type 2 youth (β˜‘ lab values) | reverses diabetes type 2 with hyperglycemia icd 10how to reverses diabetes type 2 for CD4+ T helper cells (in particular Th1 and Th17) are among the principal mediators of a pro-inflammatory environment, through the release of inflammatory cytokines (TNF-α, INF-γ, IL-17, IL-22, and IL-26 among others). CD4+CD25highForkhead Box Protein P3 (FoxP3)+ T regulatory (Treg) cells, on the other hand, are a functionally distinct cell lineage committed to exert an anti-inflammatory/immune suppressive control on innate and adaptive immune responses and they represent the most relevant cells in the body to sustain immunological homeostasis (100, 101). Treg cells function by inhibiting the activity of the pro-inflammatory counterpart CD4+ Th1 and Th17 (also referred to as T conventional or Tconv) cell subsets (102, 103). Treg-mediated suppression is based on inhibitory molecules, anti-inflammatory cytokines such as IL-10, IL-35, and Transforming Growth Factor (TGF)β and Cytotoxic T-Lymphocyte Associated protein 4 (CTLA-4), metabolic modulation and direct cytolysis of target cells (101). The transcriptional factor FoxP3 is the master regulator of Treg cell phenotype and function. Treg cells can be subdivided according to their origin into two main groups: one directly originating from the thymus, and the other arising from the peripheral conversion of naive CD4+CD25 Tconv cells (104). Peripheral Treg cell frequency ranges from 5 to 15% of CD4+ T cells, but the ratio between Treg and Tconv cells can diminish upon infection, in order to improve specific immune response activation (105). Notwithstanding the pivotal role of Treg cells in halting unwanted immune responses is certain (106), the contribution of their numerical and/or functional dysregulation to the very development and progression of human autoimmunity, and in particular autoimmune diabetes, is still to be completely clarified. The involvement and causal role of Treg cells in T2D pathogenesis is a fortiori still poorly defined. Relevant knowledge, though, has come from discovering that Treg cells are major sensors of the systemic metabolic state.

Adipose Tissue-Resident Treg Cells in Mice

In 2009, the group of Diane Mathis showed that about 10% of stromovascular fraction from the visceral adipose tissue (VAT) of C57Bl/6 lean mice fall within the lymphocyte gate, close to half of which are of the CD3+ T lineage. Among them, they revealed the presence of a unique population of Treg cells, as a much higher fraction of the CD4+ T cell compartment than usually observed in lymphoid or other non-lymphoid tissues and, importantly, their numbers were strikingly and specifically reduced at this site in insulin-resistant models of obesity (107). VAT Treg cells show a phenotype clearly distinguishable from that of their counterparts in the spleen and lymph nodes, including a distinct gene-expression profile, T cell receptor repertoire, and pattern of chemokine and chemokine receptor expression. Cytokines differentially synthesized by VAT-resident Treg and Tconv cells directly affect the synthesis of inflammatory mediators and glucose uptake by cultured adipocytes. In particular, Treg cell elevated production of the anti-inflammatory cytokine IL-10 may be essential to curb AT inflammation (107). Moreover, the residence of Treg cells into AT expose them to high concentrations of the adipocytokines, in primis leptin, discovered to halt the generation and proliferation of these cells (60, 62, 108110). Notably, Treg cells not only express the leptin receptor, but they also secrete leptin, directly contributing to metabolic homeostasis and glucose tolerance (60). Diane Mathis''Neill LA, Kishton RJ, Rathmell J. A guide to immunometabolism for immunologists. Nat Rev Immunol. (2016) 16:553–65. 10.1038/nri.2016.70 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

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