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t-regulatory cells diabetics

Ana Laura Fitas, Catarina Martins, Luís Miguel Borrego, Lurdes Lopes, Anne Jörns, Sigurd Lenzen, Catarina Limbert
AIMS/HYPOTHESIS: Type 1 diabetes (T1D) develops in distinct stages, before and after disease onset. Whether the natural course translates into different immunologic patterns is still uncertain. This study aimed at identifying peripheral immune patterns at key time-points, in T1D children undergoing remission phase. METHODS: Children with new-onset T1D and healthy age and gender-matched controls were recruited at a paediatric hospital. Peripheral blood samples were evaluated by flow cytometry at three longitudinal time-points: onset (T1), remission phase (T2) and established disease (T3)...
March 12, 2018: Pediatric Diabetes
Minglin Pan, Ying Han, Aninda Basu, Anzhi Dai, Rui Si, Conor Willson, Angela Balistrieri, Brian T Scott, Ayako Makino
Coronary microvascular rarefaction due to endothelial cell (EC) dysfunction is one of the causes of increased morbidity and mortality in diabetes. Coronary ECs in diabetes are more apoptotic due partly to mitochondrial calcium overload. This study was designed to investigate the role of hexokinase 2 (HK2, an endogenous inhibitor of voltage-dependent anion channel) in coronary endothelial dysfunction in type 2 diabetes. We used mouse coronary ECs (MCECs) isolated from type 2 diabetic mice and human coronary ECs (HCECs) from type 2 diabetic patients to examine protein levels and mitochondrial functions...
March 7, 2018: American Journal of Physiology. Cell Physiology
Rebecca J Brownlie, Rose Zamoyska, Robert J Salmond
A number of polymorphisms in immune-regulatory genes have been identified as risk factors for the development of autoimmune disease. PTPN22, that encodes a tyrosine phosphatase, has been associated with the development of several autoimmune diseases including type 1 diabetes, rheumatoid arthritis and systemic lupus erythematosus. PTPN22 regulates the activity and effector functions of multiple important immune cell types including lymphocytes, granulocytes and myeloid cells. In this review, we describe the role of PTPN22 in regulating T cell activation and effector responses...
March 7, 2018: Immunology
Yung-Luen Shih, Hsu-Feng Lu, Chiao-Wan Hsiao, Kuo-Ting Ho, Pei-Chi Chen, Chien-Ning Huang, Yuanmay Chang, Shang-Jyh Kao, Ming-Yuh Shiau, Yih-Hsin Chang
Type 2 diabetes mellitus (T2DM) is associated with chronic inflammation, suggesting the metabolic abnormalities are originated from or exacerbated by cytokine overproduction. Cytokines and counter-regulatory molecules are crucial in keeping the balance of immune responses and, therefore, are potential candidates involved in T2DM etiology, development and complications. Our previous reports identify several significant associations between the genotypes of cytokine genes and T2DM and/or the clinical lipid parameters, which strongly suggest the participation of immune-regulatory molecules in lipid metabolism...
2018: International Journal of Medical Sciences
Ling Xiao, Belinda Van't Land, Phillip A Engen, Ankur Naqib, Stefan J Green, Angie Nato, Thea Leusink-Muis, Johan Garssen, Ali Keshavarzian, Bernd Stahl, Gert Folkerts
Development of Type 1 diabetes (T1D) is influenced by non-genetic factors, such as optimal microbiome development during early life that "programs" the immune system. Exclusive and prolonged breastfeeding is an independent protective factor against the development of T1D, likely via bioactive components. Human Milk Oligosaccharides (HMOS) are microbiota modulators, known to regulate immune responses directly. Here we show that early life provision (only for a period of six weeks) of 1% authentic HMOS (consisting of both long-chain, as well as short-chain structures), delayed and suppressed T1D development in non-obese diabetic mice and reduced development of severe pancreatic insulitis in later life...
March 1, 2018: Scientific Reports
Guillaume P Andrieu, Jordan S Shafran, Jude T Deeney, Kishan R Bharadwaj, Annapoorni Rangarajan, Gerald V Denis
Obesity and its associated pathology Type 2 diabetes are two chronic metabolic and inflammatory diseases that promote breast cancer progression, metastasis, and poor outcomes. Emerging critical opinion considers unresolved inflammation and abnormal metabolism separately from obesity; settings where they do not co-occur can inform disease mechanism. In breast cancer, the tumor microenvironment is often infiltrated with T effector and T regulatory cells programmed by metabolic signaling. The pathways by which tumor cells evade immune surveillance, immune therapies, and take advantage of antitumor immunity are poorly understood, but likely depend on metabolic inflammation in the microenvironment...
March 1, 2018: Journal of Leukocyte Biology
Mehdi Soltanzadeh-Yamchi, Mehdi Shahbazi, Saeed Aslani, Mousa Mohammadnia-Afrouzi
MicroRNAs (miRNAs) are small RNA molecules with regulatory functions on the expression of genes through binding directly to target messenger RNA (mRNA) transcripts, eventuating in gene expression suppression via translational hindrance and/or target mRNA cleavage. These molecules have been established to participate in numerous critical cellular settings, including differentiation, development, and function of immune cells. As an important suppressor cell of immune system, regulatory T cells (Tregs) are important in modulating the immune homeostasis as well as tolerance to self-antigens...
February 13, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Marcelo Maia Pinheiro, Felipe Moura Maia Pinheiro, Maria Luisa Trabachin
Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease characterized by destruction of pancreatic beta cells through cell injury caused primarily by cytotoxic T lymphocytes (CD8 + ). The pathophysiological basis of T1DM seems to be an imbalance between a reduced function of T regulatory lymphocytes and an increased inflammatory activity of Th17 lymphocytes caused by increased production of inflammatory cytokines, as IL-1β, IL-6, IL-17 and IFN-gamma due to environmental factors and genetic predisposition...
February 13, 2018: International Immunopharmacology
J Zheng, S Chen, M L Albiero, G H A Vieira, J Wang, J Q Feng, D T Graves
Diabetes mellitus increases periodontitis and pathogenicity of the oral microbiome. To further understand mechanisms through which diabetes affects periodontitis, we examined its impact on periodontal ligament fibroblasts in vivo and in vitro. Periodontitis was induced by inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in normoglycemic and diabetic mice. Diabetes, induced by multiple low-dose injections of streptozotocin increased osteoclast numbers and recruitment of neutrophils to the periodontal ligament, which could be accounted for by increased CXC motif chemokine 2 (CXCL2) and receptor activator of nuclear factor kappa B ligand (RANKL) expression by these cells...
February 1, 2018: Journal of Dental Research
Keman Xu, William Y Yang, Gayani Kanchana Nanayakkara, Ying Shao, Fan Yang, Wenhui Hu, Eric T Choi, Hong Wang, Xiaofeng Yang
We conducted an experimental database analysis to determine the expression of 61 CD4+ Th subset regulators in human and murine tissues, cells, and in T-regulatory cells (Treg) in physiological and pathological conditions. We made the following significant findings: (1) adipose tissues of diabetic patients with insulin resistance upregulated various Th effector subset regulators; (2) in skin biopsy from patients with psoriasis, and in blood cells from patients with lupus, effector Th subset regulators were more upregulated than downregulated; (3) in rosiglitazone induced failing hearts in ApoE-deficient (KO) mice, various Th subset regulators were upregulated rather than downregulated; (4) aortic endothelial cells activated by proatherogenic stimuli secrete several Th subset-promoting cytokines; (5) in Treg from follicular Th (Tfh)-transcription factor (TF) Bcl6 KO mice, various Th subset regulators were upregulated; whereas in Treg from Th2-TF GATA3 KO mice and HDAC6 KO mice, various Th subset regulators were downregulated, suggesting that Bcl6 inhibits, GATA3 and HDAC6 promote, Treg plasticity; and (6) GATA3 KO, and Bcl6 KO Treg upregulated MHC II molecules and T cell co-stimulation receptors, suggesting that GATA3 and BCL6 inhibit Treg from becoming novel APC-Treg...
2018: Frontiers in Immunology
Joseph R Podojil, Iris Hecht, Ming-Yi Chiang, Ilan Vaknin, Inbal Barbiro, Amit Novik, Eyal Neria, Galit Rotman, Stephen D Miller
ILDR2 is a member of the Ig superfamily, which is implicated in tricellular tight junctions, and has a putative role in pancreatic islet health and survival. We recently found a novel role for ILDR2 in delivering inhibitory signals to T cells. In this article, we show that short-term treatment with ILDR2-Fc results in long-term durable beneficial effects in the relapsing-remitting experimental autoimmune encephalomyelitis and NOD type 1 diabetes models. ILDR2-Fc also promotes transplant engraftment in a minor mismatch bone marrow transplantation model...
February 5, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
Bogusław Nedoszytko, Małgorzata Sokołowska-Wojdyło, Joanna Renke, Magdalena Lange, Piotr Trzonkowski, Michał Sobjanek, Aneta Szczerkowska-Dobosz, Marek Niedoszytko, Aleksandra Górska, Jan Romantowski, Jarosław Skokowski, Leszek Kalinowski, Roman J Nowicki
Regulatory T cells (Tregs) represent a cell type that promotes immune tolerance to autologous components and maintains immune system homeostasis. The abnormal function of Tregs is relevant to the pathogenesis of several skin diseases like psoriasis, atopic dermatitis, systemic lupus erythematosus, cutaneous T-cell lymphomas, and skin cancer and is also important in rheumatoid arthritis, diabetes and other autoimmune diseases. In this review, we will summarize the role of mutations and/or polymorphisms of genes involved in Tregs development, and functions in the pathogenesis of selected skin diseases...
December 2017: Postȩpy Dermatologii i Alergologii
Zhen Zhao, Xiaojuan Zhang, Lili Su, Le Xu, Yong Zheng, Jian Sun
Although Interleukin-2 (IL-2) was identified almost 40 years ago, only recently low dosage IL-2 therapy is proved to be an effective approach to treat autoimmune diseases. The underlining mechanism is that IL-2 can fine-tune subsets of CD4+ T cells by promoting the development and maintenance of regulatory T cells (Treg) at low-dosage (ld) and enhance the functions of effector T cells (Teff) at high-dosage (hd). Since the successful clinical trials of IL-2 to treat patients with autoimmune diseases and inflammatory conditions, including Systemic lupus erythematosus (SLE) and Type 1 Diabetes (T1D), ld IL-2 therapy is a promising strategy to treat autoimmune diseases...
January 31, 2018: International Immunopharmacology
Julia Seyfarth, Heinz Ahlert, Joachim Rosenbauer, Christina Baechle, Michael Roden, Reinhard W Holl, Ertan Mayatepek, Thomas Meissner, Marc Jacobsen
BACKGROUND: Impaired regulatory T cell immunity plays a central role in the development of type 1 diabetes (T1D). Interleukin-2 receptor (IL-2R) signaling is essential for regulatory T cells (TREG), and cytokine-inducible SH2-containing protein (CIS) regulates IL-2R signaling as a feedback inhibitor. Previous studies identified association of CISH promoter region single nucleotide polymorphisms (SNPs) with susceptibility to infectious diseases. METHODS: Here we analyzed allele frequencies of three CISH SNPs (i...
February 6, 2018: Molecular and Cellular Pediatrics
Hannah M Brown, Ella S Green, Tiffany C Y Tan, Macarena B Gonzalez, Alice R Rumbold, M Louise Hull, Robert J Norman, Nicolle H Packer, Sarah A Robertson, Jeremy G Thompson
Diabetes has been linked with impaired fertility but the underlying mechanisms are not well defined. Here we use a streptozotocin-induced diabetes mouse model to investigate the cellular and biochemical changes in conceptus and maternal tissues that accompany hyperglycaemia. We report that streptozotocin treatment before conception induces profound intra-cellular protein β-O-glycosylation (O-GlcNAc) in the oviduct and uterine epithelium, prominent in early pregnancy. Diabetic mice have impaired blastocyst development and reduced embryo implantation rates, and delayed mid-gestation growth and development...
February 1, 2018: Scientific Reports
Haijing Wu, Yaxiong Deng, Yu Feng, Di Long, Kongyang Ma, Xiaohui Wang, Ming Zhao, Liwei Lu, Qianjin Lu
B cells have a critical role in the initiation and acceleration of autoimmune diseases, especially those mediated by autoantibodies. In the peripheral lymphoid system, mature B cells are activated by self or/and foreign antigens and signals from helper T cells for differentiating into either memory B cells or antibody-producing plasma cells. Accumulating evidence has shown that epigenetic regulations modulate somatic hypermutation and class switch DNA recombination during B-cell activation and differentiation...
January 29, 2018: Cellular & Molecular Immunology
Thalita Frutuoso Lobo, Camila de Moraes Borges, Rosiane Mattar, Caio Perez Gomes, Ana Geisa Santos de Angelo, Karen Priscilla Tezotto Pendeloski, Silvia Daher
PROBLEM: Maternal obesity is frequently associated with gestational diabetes mellitus (GDM), and immunological mechanisms seem to be involved in the physiopathology of these conditions. The aim of this study was to characterize the profile of immune cells in peripheral blood of overweight women with GDM. METHOD OF STUDY: This case-control study included 27 glucose-tolerant (controls) and 31 GDM overweight pregnant women. Flow cytometry was used to assess the number of regulatory T cells (Treg) and natural killer (NK) cells in the peripheral blood...
January 5, 2018: American Journal of Reproductive Immunology: AJRI
Isabelle Serr, Martin G Scherm, Adam M Zahm, Jonathan Schug, Victoria K Flynn, Markus Hippich, Stefanie Kälin, Maike Becker, Peter Achenbach, Alexei Nikolaev, Katharina Gerlach, Nicole Liebsch, Brigitta Loretz, Claus-Michael Lehr, Benedikt Kirchner, Melanie Spornraft, Bettina Haase, James Segars, Christoph Küper, Ralf Palmisano, Ari Waisman, Richard A Willis, Wan-Uk Kim, Benno Weigmann, Klaus H Kaestner, Anette-Gabriele Ziegler, Carolin Daniel
Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3 + regulatory T cell (T reg ) induction in vitro...
January 3, 2018: Science Translational Medicine
Yan Yang, Lixiu Liu, Beibei Liu, Qi Li, Zhe Wang, Sitong Fan, He Wang, Liandi Wang
Gestational diabetes mellitus (GDM) is a metabolic and low-grade inflammatory disease most commonly found in pregnant women with high body mass index and non-Caucasian ethnicities; however, not all women of high-risk groups develop GDM. We hypothesized that regulatory T cells (Tregs) might present a role in suppressing GDM development. To this end, 55 high-risk women at early pregnancy (first trimester) were recruited, and 21 of them developed GDM while the other 34 did not. Compared to those subjects who did not develop GDM (non-GDM), the patients who developed GDM presented reduced levels of Tregs and elevated levels of serum interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha)...
January 3, 2018: DNA and Cell Biology
Maran L Sprouse, Ivan Shevchenko, Marissa A Scavuzzo, Faith Joseph, Thomas Lee, Samuel Blum, Malgorzata Borowiak, Matthew L Bettini, Maria Bettini
Regulatory T cells (Tregs) use a distinct TCR repertoire and are more self-reactive compared with conventional T cells. However, the extent to which TCR affinity regulates the function of self-reactive Tregs is largely unknown. In this study, we used a two-TCR model to assess the role of TCR affinity in Treg function during autoimmunity. We observed that high- and low-affinity Tregs were recruited to the pancreas and contributed to protection from autoimmune diabetes. Interestingly, high-affinity cells preferentially upregulated the TCR-dependent Treg functional mediators IL-10, TIGIT, GITR, and CTLA4, whereas low-affinity cells displayed increased transcripts for Areg and Ebi3 , suggesting distinct functional profiles...
February 1, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
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