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Scooped by
Gilbert C FAURE
November 14, 2017 1:33 PM
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National Academy of Sciences
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Scooped by
Gilbert C FAURE
November 7, 2017 11:36 AM
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Type 1 diabetes (T1D) is one of the most common and severe chronic diseases affecting both children and adults. The aetiology of the disease remains unknown, and thus far no ‘true’ cure for thos
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Suggested by
LIGHTING
November 6, 2017 1:40 PM
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EULAR and ACR present a draft of new SLE Classification criteria at the 2017 ACR/ARHP Annual Meeting.
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Scooped by
Gilbert C FAURE
November 6, 2017 1:15 PM
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Article Citation: Steven C. Weindorf and John Karl Frederiksen (2017) IgG4-Related Disease: A Reminder for Practicing Pathologists. Archives of Pathology & Laboratory Medicine: November 2017, Vol. 141, No. 11, pp. 1476-1483. https://doi.org/10.5858/arpa.2017-0257-RA
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Scooped by
Gilbert C FAURE
November 5, 2017 3:37 AM
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Portal for open access research theses. DART-Europe is a partnership of research libraries and library consortia who are working together to improve global access to European research theses. The DART-Europe partners help to provide researchers with a single European Portal for the discovery of Electronic Theses and Dissertations (ETDs).
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Scooped by
Gilbert C FAURE
November 2, 2017 12:55 PM
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Scooped by
Gilbert C FAURE
October 30, 2017 2:52 PM
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Scooped by
Gilbert C FAURE
October 27, 2017 4:41 AM
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Scooped by
Gilbert C FAURE
October 25, 2017 1:17 PM
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Immunology and Cell Biology focuses on the general functioning of the immune system in its broadest sense, with a particular emphasis on its cell biology. Areas that are covered include but are not limited to: Cellular immunology, Innate and adaptive immunity, Immune responses to pathogens,Tumour immunology,Immunopathology, Immunotherapy, Immunogenetics, Immunological studies in humans and model organisms (including mouse, rat, Drosophila etc)
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Scooped by
Gilbert C FAURE
October 16, 2017 10:27 AM
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Clinical Implications of Basic Research from The New England Journal of Medicine — Celiac Disease and Autoimmunity — The Missing Ingredient
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Scooped by
Gilbert C FAURE
October 13, 2017 9:40 AM
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Introduction Recent evidence has demonstrated that, among other factors, dysbiosis (imbalances in the composition and function of the gut microbiota) may be relevant in the development of type 1 diabetes (T1D). Thus, gut microbiota may be a target for improving outcomes in subjects with T1D. The aim of the study is to examine the effects of Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12 on beta-cell function in children with newly diagnosed T1D. Methods and analysis A total of 96 children aged 8 to 17 years with newly diagnosed T1D, confirmed by clinical history and the presence of at least one positive autoantibody, will be enrolled in a double-blind, randomised, placebo-controlled trial in which they will receive L. rhamnosus GG and B. lactis Bb12 at a dose of 109 colony-forming units or an identically appearing placebo, orally, once daily, for 6 months. The follow-up will be for 12 months. The primary outcome measures will be the area under the curve of the C-peptide level during 2-hour responses to a mixed meal. Ethics and dissemination The Bioethics Committee approved the study protocol. The findings of this trial will be submitted to a peer-reviewed paediatric journal. Abstracts will be submitted to relevant national and international conferences. Trial registration number NCT03032354; Pre-results.
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Scooped by
Gilbert C FAURE
October 10, 2017 8:29 AM
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Scientists have discovered that the onset of type 1 diabetes is preceded by modification of MAIT lymphocytes. These cells—associated with mucosae and able to recognize elements of the microbiota—could therefore serve as new biomarkers for early detection and prevention of the illness.
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Scooped by
Gilbert C FAURE
October 9, 2017 7:59 AM
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Thermo Fisher Scientific has a job opportunity for a Training Specialist for Autoimmunity in Remote / Field,
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Suggested by
Société Francaise d'Immunologie
November 14, 2017 1:29 PM
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Few concepts in recent years have garnered more disease research attention than that of the intestinal (i.e. ‘gut’) microbiome. This emerging interest has included investigations of the microbiome'
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Scooped by
Gilbert C FAURE
November 7, 2017 9:31 AM
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Background/Purpose: Evidence supports the existence of different sub-phenotypes and the pivotal role of cytokines and autoantibodies in systemic lupus erythematosus (SLE). Cytokines interact in a highly complex network. Thus, understanding how these complex non-linear processes are connected and observed in real-life settings is a major challenge. Cluster approaches may assist in the identification of these …
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Scooped by
Gilbert C FAURE
November 6, 2017 1:30 PM
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Read a free sample or buy Antiphospholipid Syndrome by Laurent Phialy, Stéphane Zuily & Doruk Erkan. You can read this book with iBooks on your iPhone, iPad, iPod touch, or Mac.
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Scooped by
Gilbert C FAURE
November 6, 2017 1:11 PM
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The transcription factor NFAT1 plays a pivotal role in the homeostasis of T lymphocytes. However, its functional importance in non-CD4+ T cells, especially in systemic immune disorders, is largely unknown. In this study, we report that NFAT1 regulates dendritic cell (DC) tolerance and suppresses systemic autoimmunity using the experimental autoimmune myasthenia gravis (EAMG) as a model. Myasthenia gravis and EAMG are T cell–dependent, Ab-mediated autoimmune disorders in which the acetylcholine receptor is the major autoantigen. NFAT1-knockout mice showed higher susceptibility to EAMG development with enhanced Th1/Th17 cell responses. NFAT1 deficiency led to a phenotypic alteration of DCs that show hyperactivation of NF-κB–mediated signaling pathways and enhanced binding of NF-κB (p50) to the promoters of IL-6 and IL-12. As a result, NFAT1-knockout DCs produced much higher levels of proinflammatory cytokines such as IL-1β, IL-6, IL-12, and TNF-α, which preferentially induce Th1/Th17 cell differentiation. Our data suggest that NFAT1 may limit the hyperactivation of the NF-κB–mediated proinflammatory response in DCs and suppress autoimmunity by serving as a key regulator of DC tolerance.
Autoimmune lymphoproliferative syndrome (ALPS) is an inherited syndrome characterized by abnormal lymphocyte survival caused by failure of apoptotic mechanisms to maintain lymphocyte homeostasis. This failure leads to the clinical manifestations of non-infectious and non-malignant lymphadenopathy, splenomegaly, and autoimmune pathology, most commonly, autoimmune cytopenias. Since ALPS was first characterized in the early 1990s, insights in disease biology have improved both diagnosis and management of this syndrome. Sirolimus is the best-studied and most effective corticosteroid-sparing therapy for ALPS and should be considered first-line for patients in need of chronic treatment. This review highlights practical clinical considerations for the diagnosis and management of ALPS. Further studies could reveal new proteins and regulatory pathways that are critical for lymphocyte activation and apoptosis.
Via Krishan Maggon
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Suggested by
LIGHTING
November 1, 2017 3:42 PM
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Suggested by
Société Francaise d'Immunologie
October 30, 2017 5:28 AM
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Myeloperoxidase (MPO) anti-neutrophil cytoplasmic Ab (ANCA)–associated vasculitis results from autoimmunity to MPO. IL-17A plays a critical role in generating this form of autoimmune injury but its cell of origin is uncertain. We addressed the hypothesis that IL-17A–producing γδ T cells are a nonredundant requisite in the development of MPO autoimmunity and glomerulonephritis (GN). We studied MPO-ANCA GN in wild type, αβ, or γδ T cell–deficient (C57BL/6, βTCR−/− , and δTCR −/− respectively) mice. Both T cell populations played important roles in the generation of autoimmunity to MPO and GN. Humoral autoimmunity was dependent on intact αβ T cells but was unaffected by γδ T cell deletion. Following MPO immunization, activated γδ T cells migrate to draining lymph nodes. Studies in δTCR −/− and transfer of γδ T cells to δTCR −/− mice show that γδ T cells facilitate the generation of anti-MPO autoimmunity and GN. δTCR −/− mice that received IL-17A −/− γδ T cells demonstrate that the development of anti-MPO autoimmunity and GN are dependent on γδ T cell IL-17A production. Finally, transfer of anti-MPO CD4+ T cell clones to naive δTCR −/− and wild type mice with planted glomerular MPO shows that γδ T cells are also necessary for recruitment of anti-MPO αβ CD4+ effector T cells. This study demonstrates that IL-17A produced by γδ T cells plays a critical role in the pathogenesis of MPO-ANCA GN by promoting the development of MPO-specific αβ T cells.
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Scooped by
Gilbert C FAURE
October 27, 2017 4:40 AM
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The aim of this study is to compare the rates of clinically relevant and clinically irrelevant neuronal autoantibodies among patients presenting with new neurological symptoms. We reviewed 401 neurolo
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Scooped by
Gilbert C FAURE
October 16, 2017 2:14 PM
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Scooped by
Gilbert C FAURE
October 14, 2017 10:07 AM
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A hallmark of systemic lupus erythematosus is high titers of circulating autoantibodies. Recently, a novel CD11c+ B-cell subset has been identified that is critical for the development of autoimmunity. However, the role of CD11c+ B cells in the development of lupus is unclear. Chronic graft-versus-host disease (cGVHD) is a lupus-like syndrome with high autoantibody production. The purpose of this study was to explore the role of CD11c+ B cells in the pathogenesis of lupus in cGVHD mice. cGVHD was induced by an intraperitoneal injection of 5 × 107 Bm12 splenocytes into B6 mice. Flow cytometry was used to analyze mice splenocytes and human samples. Magnetic beads were used to isolate mice B cells. Gene expression was determined by real-time quantitative polymerase chain reaction (RT-qPCR). Enzyme-linked immunosorbent assay (ELISA) was used to detect antibodies in serum and supernatants. The percentage and absolute number of CD11c+ B cells was increased in cGVHD-induced lupus, with elevated levels of antichromatin immunoglobulin (Ig)G and IgG2a in sera. CD11c+ plasma cells from cGVHD mice produced large amounts of antichromatin IgG2a upon stimulation. Depletion of CD11c+ B cells reduced antichromatin IgG and IgG2a production. T-bet was upregulated in CD11c+ B cells. Knockout of T-bet in B cells alleviated cGVHD-induced lupus. Importantly, the percentage of T-bet+CD11c+ B cells increased in lupus patients and positively correlated with serum antichromatin levels. T-bet+CD11c+ B cells promoted high antichromatin IgG production in the lupus-like disease model cGVHD. In lupus patients, the percentage of T-bet+CD11c+ B cells was elevated and positively correlated with antichromatin antibodies. The findings provide potential therapeutic insight into lupus disease treatment.
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Scooped by
Gilbert C FAURE
October 12, 2017 4:48 AM
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A University of Birmingham academic has led the authorship of the UK's first guideline on the care of adults with systemic lupus erythematosus (lupus).
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Scooped by
Gilbert C FAURE
October 9, 2017 8:00 AM
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PDN information about Pandas
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