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https://www.readbyqxmd.com/read/29315988/impaired-treg-and-nk-cells-profile-in-overweight-women-with-gestational-diabetes-mellitus
#1
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
https://www.readbyqxmd.com/read/29298866/a-mirna181a-nfat5-axis-links-impaired-t-cell-tolerance-induction-with-autoimmune-type-1-diabetes
#2
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 (Treg) induction in vitro...
January 3, 2018: Science Translational Medicine
https://www.readbyqxmd.com/read/29298097/functional-defects-of-regulatory-t-cell-through-interleukin-10-mediated-mechanism-in-the-induction-of-gestational-diabetes-mellitus
#3
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
https://www.readbyqxmd.com/read/29282307/cutting-edge-low-affinity-tcrs-support-regulatory-t-cell-function-in-autoimmunity
#4
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...
December 27, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29259102/altered-homeostasis-and-development-of-regulatory-t-cell-subsets-represent-an-il-2r-dependent-risk-for-diabetes-in-nod-mice
#5
Connor J Dwyer, Allison L Bayer, Carmen Fotino, Liping Yu, Cecilia Cabello-Kindelan, Natasha C Ward, Kevin H Toomer, Zhibin Chen, Thomas R Malek
The cytokine interleukin-2 (IL-2) is critical for the functions of regulatory T cells (Tregs). The contribution of polymorphisms in the gene encoding the IL-2 receptor α subunit (IL2RA), which are associated with type 1 diabetes, is difficult to determine because autoimmunity depends on variations in multiple genes, where the contribution of any one gene product is small. We investigated the mechanisms whereby a modest reduction in IL-2R signaling selectively in T lymphocytes influenced the development of diabetes in the NOD mouse model...
December 19, 2017: Science Signaling
https://www.readbyqxmd.com/read/29249872/taenia-crassiceps-antigens-control-experimental-type-1-diabetes-by-inducing-alternatively-activated-macrophages
#6
Arlett Espinoza-Jiménez, Roberto De Haro, Luis I Terrazas
Type 1 diabetes (T1D) is an autoimmune disease caused by the selective destruction of the pancreatic β-cells, causing inability to produce insulin. Proinflammatory cytokines such as IL-1β, IL-6, TNF-α, IFN-γ, IL-12, IL-17, and NO can be released by CD4 and CD8+ lymphocytes as well as by classically activated macrophages (CAMϕs), which are important in the development of T1D. Helminth infections have been shown to prevent T1D, mainly through Th2-biased responses and increased recruitment of regulatory cell populations...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/29215791/protective-effects-of-carbonyl-iron-against-multiple-low-dose-streptozotocin-induced-diabetes-in-rodents
#7
Milica Vujicic, Tamara Saksida, Marija Mostarica Stojkovic, Neda Djedovic, Ivana Stojanovic, Stanislava Stosic-Grujicic
Particulate adjuvants have shown increasing promise as effective, safe, and durable agents for the stimulation of immunity, or alternatively, the suppression of autoimmunity. Here we examined the potential of the adjuvant carbonyl iron (CI) for the modulation of organ-specific autoimmune disease-type 1 diabetes (T1D). T1D was induced by multiple low doses of streptozotocin (MLDS) that initiates beta cell death and triggers immune cell infiltration into the pancreatic islets. The results of this study indicate that the single in vivo application of CI to MLDS-treated DA rats, CBA/H mice, or C57BL/6 mice successfully counteracted the development of insulitis and hyperglycemia...
December 7, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29209330/the-enigma-of-heat-shock-proteins-in-immune-tolerance
#8
REVIEW
Willem van Eden, Manon A A Jansen, Irene Ludwig, Peter van Kooten, Ruurd van der Zee, Femke Broere
The fundamental problem of autoimmune diseases is the failure of the immune system to downregulate its own potentially dangerous cells, which leads to destruction of tissue expressing the relevant autoantigens. Current immunosuppressive therapies offer relief but fail to restore the basic condition of self-tolerance. They do not induce long-term physiological regulation resulting in medication-free disease remissions. Heat shock proteins (HSPs) have shown to possess the capacity of inducing lasting protective immune responses in models of experimental autoimmune diseases...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29193502/foxp3-mutations-causing-early-onset-insulin-requiring-diabetes-but-without-other-features-of-immune-dysregulation-polyendocrinopathy-enteropathy-x-linked-syndrome
#9
Jessica L Hwang, Soo-Young Park, Honggang Ye, May Sanyoura, Ashley N Pastore, David Carmody, Daniela Del Gaudio, Janna F Wilson, Craig L Hanis, Xiaoming Liu, Gil Atzmon, Benjamin Glaser, Louis H Philipson, Siri Atma W Greeley
Diabetes occurs in 1/90 000 to 1/160 000 births and when diagnosed under 6 months of age is very likely to have a primary genetic cause. FOXP3 encodes a transcription factor critical for T regulatory cell function and mutations are known to cause "immune dysregulation, polyendocrinopathy (including insulin-requiring diabetes), enteropathy, X-linked" (IPEX) syndrome. This condition is often fatal unless patients receive a bone-marrow transplant. Here we describe the phenotype of male neonates and infants who had insulin-requiring diabetes without other features of IPEX syndrome and were found to have mutations in FOXP3...
November 29, 2017: Pediatric Diabetes
https://www.readbyqxmd.com/read/29181000/prenatal-administration-of-betamethasone-causes-changes-in-the-t-cell-receptor-repertoire-influencing-development-of-autoimmunity
#10
Anna Gieras, Christina Gehbauer, David Perna-Barrull, Jan Broder Engler, Ines Diepenbruck, Laura Glau, Simon A Joosse, Nora Kersten, Stefanie Klinge, Hans-Willi Mittrücker, Manuel A Friese, Marta Vives-Pi, Eva Tolosa
Prenatal glucocorticoids are routinely administered to pregnant women at risk of preterm delivery in order to improve survival of the newborn. However, in half of the cases, birth occurs outside the beneficial period for lung development. Glucocorticoids are potent immune modulators and cause apoptotic death of immature T cells, and we have previously shown that prenatal betamethasone treatment at doses eliciting lung maturation induce profound thymocyte apoptosis in the offspring. Here, we asked if there are long-term consequences on the offspring's immunity after this treatment...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29176645/t-cell-receptor-%C3%AE-chains-display-abnormal-shortening-and-repertoire-sharing-in-type-1-diabetes
#11
Iria Gomez-Tourino, Yogesh Kamra, Roman Baptista, Anna Lorenc, Mark Peakman
Defects in T cell receptor (TCR) repertoire are proposed to predispose to autoimmunity. Here we show, by analyzing >2 × 108 TCRB sequences of circulating naive, central memory, regulatory and stem cell-like memory CD4+ T cell subsets from patients with type 1 diabetes and healthy donors, that patients have shorter TCRB complementarity-determining region 3s (CDR3), in all cell subsets, introduced by increased deletions/reduced insertions during VDJ rearrangement. High frequency of short CDR3s is also observed in unproductive TCRB sequences, which are not subjected to thymic culling, suggesting that the shorter CDR3s arise independently of positive/negative selection...
November 27, 2017: Nature Communications
https://www.readbyqxmd.com/read/29171836/crig-a-tissue-resident-macrophage-specific-immune-checkpoint-molecule-promotes-immunological-tolerance-in-nod-mice-via-a-dual-role-in-effector-and-regulatory-t-cells
#12
Xiaomei Yuan, Bi-Huei Yang, Yi Dong, Asami Yamamura, Wenxian Fu
How tissue-resident macrophages (TRM) impact adaptive immune responses remains poorly understood. We report novel mechanisms by which TRMs regulate T cell activities at tissue sites. These mechanisms are mediated by the complement receptor of immunoglobulin family (CRIg). Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg+ TRMs formed a protective barrier surrounding pancreatic islets. Genetic ablation of CRIg exacerbated islet inflammation and local T cell activation. CRIg exhibited a dual function of attenuating early T cell activation and promoting the differentiation of Foxp3+ regulatory (Treg) cells...
November 24, 2017: ELife
https://www.readbyqxmd.com/read/29159964/blocking-antibodies-induced-by-allergen-specific-immunotherapy-ameliorate-allergic-airway-disease-in-a-human-mouse-chimeric-model
#13
Caterina Vizzardelli, Miriam Gindl, Simone Roos, Christian Möbs, Birgit Nagl, Felix Zimmann, Veronika Sexl, Lukas Kenner, Alina Neunkirchner, Gerhard J Zlabinger, Winfried F Pickl, Wolfgang Pfützner, Barbara Bohle
BACKGROUND: Allergen-specific immunotherapy (AIT) induces specific blocking antibodies (Ab) which are claimed to prevent IgE-mediated reactions to allergens. Additionally, AIT modulates cellular responses to allergens, e.g. by desensitizing effector cells, inducing regulatory T and B lymphocytes and immune deviation. It is still enigmatic which of these mechanisms mediate(s) clinical tolerance. We sought to address the role of AIT-induced blocking Ab separately from cellular responses in a chimeric human/mouse model of respiratory allergy...
November 21, 2017: Allergy
https://www.readbyqxmd.com/read/29155454/harnessing-the-power-of-regulatory-t-cells-to-control-autoimmune-diabetes-overview-and-perspective
#14
REVIEW
Hua Yu, Ricardo Paiva, Richard A Flavell
Type 1 diabetes (T1D) is a T cell-mediated autoimmune disease resulting in islet β-cell destruction, hypoinsulinemia, and severely altered glucose homeostasis. Although the mechanisms that initiate T1D still remain elusive, a breakdown of immune tolerance between effector T cells (Teff) and regulatory T cells (Treg) is considered to be the crucial component leading to autoimmunity. As such, strategies have been developed to boost the number and/or function of Treg in the hope of specifically hampering the pathogenic Teff activity...
November 20, 2017: Immunology
https://www.readbyqxmd.com/read/29149782/frequency-of-circulatory-regulatory-immune-cells-in-iranian-patients-with-type-1-diabetes
#15
Tahereh Khamehchian, Eqlim Nemati, Marziyeh Jazayeri, Shirin Azimi, Hassan Nikoueinejad, Hossein Akbari, Behnaz Irandoust
Type 1 diabetes (T1D) is the result of the autoimmune destruction of insulin-producing beta cells. Regulatory T cells (Tregs) and plasmacytoid dendritic cells (PDCs) act as mediators of peripheral tolerance. We investigated the possible alterations of such cells in peripheral blood of patients with T1D compared to normal individuals. This comparison may lead to a better understanding of the immunopathogenesis processes involved in T1D. 92 participants, including 49 patients with T1D and 43 healthy controls were studied...
October 2017: Iranian Journal of Allergy, Asthma, and Immunology
https://www.readbyqxmd.com/read/29141759/cell-type-specific-immunomodulation-induced-by-helminthes-effect-on-metainflammation-insulin-resistance-and-type-2-diabetes
#16
REVIEW
Vivekanandhan Aravindhan, Gowrishankar Anand
Recent epidemiological studies have documented an inverse relationship between the decreasing prevalence of helminth infections and the increasing prevalence of metabolic diseases ("metabolic hygiene hypothesis"). Chronic inflammation leading to insulin resistance (IR) has now been identified as a major etiological factor for a variety of metabolic diseases other than obesity and Type-2 diabetes (metainflammation). One way by which helminth infections such as filariasis can modulate IR is by inducing a chronic, nonspecific, low-grade, immune suppression mediated by modified T-helper 2 (Th2) response (induction of both Th2 and regulatory T cells) which can in turn suppress the proinflammatory responses and promote insulin sensitivity (IS)...
December 2017: American Journal of Tropical Medicine and Hygiene
https://www.readbyqxmd.com/read/29136611/gut-microbiota-in-health-and-disease
#17
Yuichiro Yamashiro
Intestinal regulatory T (Treg) cells are critical to maintaining immune tolerance to dietary antigens and gut microbiota. This paper reviews several papers on this topic that were recently published by Japanese researchers. Specifically, Prof. K. Honda and his group have found that commensal microbiota capable of metabolizing butyrate induces the differentiation of colonic Treg cells. In a separate work, Prof. Y. Yokoyama and his group used a novel, culture-independent analytical method (the Yakult Intestinal Flora-Scan) for detection of bacteria in the bloodstream...
November 14, 2017: Annals of Nutrition & Metabolism
https://www.readbyqxmd.com/read/29133420/resident-macrophages-of-pancreatic-islets-have-a-seminal-role-in-the-initiation-of-autoimmune-diabetes-of-nod-mice
#18
Javier A Carrero, Derrick P McCarthy, Stephen T Ferris, Xiaoxiao Wan, Hao Hu, Bernd H Zinselmeyer, Anthony N Vomund, Emil R Unanue
Treatment of C57BL/6 or NOD mice with a monoclonal antibody to the CSF-1 receptor resulted in depletion of the resident macrophages of pancreatic islets of Langerhans that lasted for several weeks. Depletion of macrophages in C57BL/6 mice did not affect multiple parameters of islet function, including glucose response, insulin content, and transcriptional profile. In NOD mice depleted of islet-resident macrophages starting at 3 wk of age, several changes occurred: (i) the early entrance of CD4 T cells and dendritic cells into pancreatic islets was reduced, (ii) presentation of insulin epitopes by dispersed islet cells to T cells was impaired, and (iii) the development of autoimmune diabetes was significantly reduced...
November 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29123529/t-cell-mediated-chronic-inflammatory-diseases-are-candidates-for-therapeutic-tolerance-induction-with-heat-shock-proteins
#19
REVIEW
Ariana Barbera Betancourt, Qingkang Lyu, Femke Broere, Alice Sijts, Victor P M G Rutten, Willem van Eden
Failing immunological tolerance for critical self-antigens is the problem underlying most chronic inflammatory diseases of humans. Despite the success of novel immunosuppressive biological drugs, the so-called biologics, in the treatment of diseases such rheumatoid arthritis (RA) and type 1 diabetes, none of these approaches does lead to a permanent state of medicine free disease remission. Therefore, there is a need for therapies that restore physiological mechanisms of self-tolerance. Heat shock proteins (HSPs) have shown disease suppressive activities in many models of experimental autoimmune diseases through the induction of regulatory T cells (Tregs)...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29123516/avidity-and-bystander-suppressive-capacity-of-human-regulatory-t-cells-expressing-de-novo-autoreactive-t-cell-receptors-in-type-1-diabetes
#20
Wen-I Yeh, Howard R Seay, Brittney Newby, Amanda L Posgai, Filipa Botelho Moniz, Aaron Michels, Clayton E Mathews, Jeffrey A Bluestone, Todd M Brusko
The ability to alter antigen specificity by T-cell receptor (TCR) or chimeric antigen receptor (CAR) gene transfer has facilitated personalized cellular immune therapies in cancer. Inversely, this approach can be harnessed in autoimmune settings to attenuate inflammation by redirecting the specificity of regulatory T cells (Tregs). Herein, we demonstrate efficient protocols for lentiviral gene transfer of TCRs that recognize type 1 diabetes-related autoantigens with the goal of tissue-targeted induction of antigen-specific tolerance to halt β-cell destruction...
2017: Frontiers in Immunology
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