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1,355 results for “Autoimmunity”
The Relationship Between COVID-19 and Autoimmune Diseases, Lessons From Practice
ClinicalTrials.gov study NCT04558203. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Autoimmune Gastrointestinal Dysmotility: Symptoms, Pathogenesis and Treatment
ClinicalTrials.gov study NCT04859829. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Analysis of B Cells From Autoimmune Individuals
ClinicalTrials.gov study NCT02747277. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Immunomodulatory Therapy in Women With Autoimmune Premature Ovarian Insufficiency
ClinicalTrials.gov study NCT05586737. IPD Sharing: NO. Countries: 1. Publications: 0.
RNAseq of tolerized auroreactive RBC-specific CD4 T cells, HODxOTII murine model of autoimmune hemolytic anemia (AIHA)
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Data from: Autoimmune encephalitis: a costly condition
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NanoString autoimmune profiling panel normalized linear counts and summary of statistical analyses
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Data from: Identification of novel, clinically correlated autoantigens in the monogenic autoimmune syndrome APS1 by PhIP-Seq
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Raw data related to: Molecular Mechanisms Controlling Foxp3 Expression in Health and Autoimmunity: From Epigenetic to Post-translational Regulation.
<p><strong>Abstract</strong></p> <p>The discovery of the transcription factor Forkhead box-p3 (Foxp3) has shed fundamental insights into the understanding of the molecular determinants leading to generation and maintenance of T regulatory (Treg) cells, a cell population with a key immunoregulatory role. Work over the past few years has shown that fine-tuned transcriptional and epigenetic events are required to ensure stable expression of Foxp3 in Treg cells. The equilibrium between phenotypic plasticity and stability of Treg cells is controlled at the molecular level by networks of transcription factors that bind regulatory sequences, such as enhancers and promoters, to regulate Foxp3 expression. Recent reports have suggested that specific modifications of DNA and histones are required for the establishment of the chromatin structure in conventional CD4+ T (Tconv) cells for their future differentiation into the Treg cell lineage. In this review, we discuss the molecular events that control Foxp3 gene expression and address the associated alterations observed in human diseases. Also, we explore how Foxp3 influences the gene expression programs in Treg cells and how unique properties of Treg cell subsets are defined by other transcription factors.</p> <p> </p> <p><strong>Progetto giovani ricercatori</strong>[GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"</p> <p> </p> <p> </p> <p> </p>
Raw data related to: "Transcriptional Regulators of T Helper 17 Cell Differentiation in Health and Autoimmune Diseases"
<p><strong>Introduction</strong></p> <p>T helper (Th) 17 cells are a subtype of CD4 T lymphocytes characterized by the expression of retinoic acid-receptor (RAR)-related orphan receptor (ROR)γt transcription factor, encoded by gene <em>Rorc</em>. These cells are implicated in the pathology of autoimmune inflammatory disorders as well as in the clearance of extracellular infections. The main function of Th17 cells is the production of cytokine called interleukin (IL)-17A.</p> <p><strong>Methods</strong></p> <p>We described the lineage defining transcription factor RORγt and other factors that regulate transcription of <em>Il17a, Rorc </em>and Th17-related genes, such as Il17f, Il21, Il23r, which may positively or negatively influence their expression.</p> <p><strong>Results</strong></p> <p>We discussed the potential new therapeutic approaches for Th17-related diseases targeting these transcription factors. The wide knowledge of transcriptional regulators of Th17 cells is crucial for the better understanding of the pathogenic role of these cells and for development of therapeutic strategies aimed at fighting Th17-related diseases.</p>
Data from: Paraneoplastic neuronal intermediate filament autoimmunity
Objective: To describe paraneoplastic neuronal intermediate filament (NIF) autoimmunity. Methods: Archived patient and control serum and CSF specimens were evaluated by tissue-based indirect immunofluorescence assay (IFA). Autoantigens were identified by western blot and mass spectrometry. NIF specificity was confirmed by dual tissue section staining and 5 recombinant NIF-specific HEK293 cell based assays (CBAs, for alpha internexin, neurofilament light [NF-L], medium, or heavy chain, and peripherin). NIF-IgGs were correlated with neurological syndromes and cancers. Results: Among 65 patients, NIF-IgG positive by IFA and CBAs, 33 were female (51%). Median symptom-onset age was 62 years (range, 18-88). Patients fell into 2 groups, defined by the presence of NF-L-IgG (21 patients, who mostly had ≥4 NIF-IgGs detected) or its absence (44 patients, who mostly had ≤2 NIF-IgGs detected). Among NF-L-IgG positive patients, 19/21 had ≥1 subacute onset CNS disorders: cerebellar ataxia (11), encephalopathy (11); myelopathy (2). Cancers were detected in 16 of 21 patients (77%): carcinomas of neuroendocrine lineage (10) being most common (small cell [5], Merkel cell [3], other neuroendocrine [2]). Two of 257 controls (0.8%, both with small cell carcinoma) were positive by both IFA and CBA. Five of 7 patients with immunotherapy data improved. By comparison, the 44 NF-L-IgG negative patients had findings of unclear significance: diverse nervous system disorders (p=0.006), as well as limited (p=0.003) and more diverse (p<0.0001) cancer accompaniments. Conclusions: NIF-IgG detection by IFA, with confirmatory CBA testing that yields a profile including NF-L-IgG, defines a paraneoplastic CNS disorder (usually ataxia or encephalopathy) accompanying neuroendocrine lineage neoplasia.
Mental disease and risk of autoimmune disease: a Mendelian randomization study
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Immune cell parameters found to be impacted in patients with autoimmune and autoinflammatory disorders enrolled in the Transimmunom study.
<p>Expanding upon the Transimmunom clinical trial, we gathered peripheral blood samples from 443 patients enrolled between 2015 and 2022, who were afflicted with 15 distinct autoimmune or autoinflammatory diseases or related conditions. Additionally, blood samples were collected from 71 healthy volunteers to establish a reference condition. The screened disorders spanned a spectrum from purely autoinflammatory to purely autoimmune diseases, encompassing various levels of disorder activities without a specific threshold. The disorders examined included arthritis conditions such as Behçet's disease (BD; n=38), knee osteoarthritis (OA; n=45), rheumatoid arthritis (RA; n=91), spondylarthritis (SA; n=58), and systemic lupus erythematosus (SLE; n=33). Blood vessel disorders, such as Antiphospholipid syndrome (APLS; n=23), Churg-Strauss's disease (CS; n=6), Granulomatosis with polyangiitis (GPA; n=14), and Takayasu arteritis (TA; n=22), were also included. Metabolic disorders like Type 1 Diabetes (T1D; n=60) and Type 2 Diabetes (T2D; n=27), muscle disorder (Myositis; n=4), inflammatory bowel diseases (IBD) like Crohn's disease (CD; n=10) and ulcerative colitis (UC; n=5), as well as IBD-like diseases including Familial Mediterranean Fever (FMF; n=7), were part of the study.</p><p>To analyze the patient blood samples, we utilized 12 flow cytometry panels, each consisting of 10 cell markers. We introduced an extra panel specifically designed to identify the primary immune cell populations. This panel featured numeration beads, enabling the determination of absolute counts for all populations. It served as a reference tube, facilitating the calculation of absolute counts in all other panels through extrapolation from shared populations. In total, we analyzed more than 600 innate and adaptive immune cell parameters (both absolute cell counts and percentages) from patient's blood.</p><p>The provided data encompasses significant flow cytometry data related to the Transimmunom study. This dataset specifically details the values of 224 cell parameters that exhibit significant differential abundance in at least one disease when compared to samples from healthy volunteers. Both Cliff's Delta effect size and two-way non-parametric Wilcoxon test were used to identify cell parameters significantly differentially abundant between conditions. Cell parameters with an absolute value of Cliff's Delta effect size higher than 0.33 and with a p-value lower than 0.05 were considered statistically significant. </p><p>The provided file is formatted as a tab-separated file. Each row corresponds to a specific cell parameter, either representing cell percentage or absolute cell count. Each column corresponds to a distinct patient, identified by the disease name and anonymous identifier.</p>
Autoimmunity in monogenic combined immune deficiencies with associated or syndromic features
<p><strong><em>Abstract</em></strong></p> <p><strong><em>Background</em></strong><strong>:</strong> Combined immune deficiencies (CIDs) with associated or syndromic features are a highly heterogeneous subgroup of inherited immune disorders. These patients represent specific clinical complications with an increased risk of autoimmune conditions.</p> <p><strong><em>Methods</em></strong><strong>:</strong> We analyzed data of monogenic patients with syndromic CIDs adopted from the Iranian inborn errors of immunity registry up to January 2022. A comprehensive comparison in terms of demographic, clinical, and immunological features was performed between patients with and without autoimmunity and also among four mutation groups with the most registered cases including ataxia-telangiectasia mutated (<em>ATM</em>), <em>STAT3 AD (LOF)</em> , <em>DNMT3B/ ZBTB24, </em>and <em>WAS</em> mutations.</p> <p><strong><em>Results</em></strong><strong>:</strong> A total of 137 patients with monogenic syndromic CIDs were included. Most commonly mutated genes were the <em>ATM</em> [80 (58.4%)] and <em>STAT3</em> [19 (13.9%)], followed by <em>DNMT3B</em> [11 (8%)], and <em>WAS</em> [11 (8%)]. More than 18% of all patients with syndromic CIDs, including most <em>DNMT3B / ZBTB24</em> mutations patients, were clinically diagnosed with antibody deficiencies before genetic evaluation. Patients with <em>ATM</em> and <em>WAS </em>mutations had the latest age of onset and the lowest age of diagnosis, respectively. Autoimmune disorders were diagnosed in 24 patients at a median age of 3.5 (2.6-6.0) years, 70.6% of which were diagnosed prior to the diagnosis of immunodeficiency. Lymphoproliferation, particularly hepatosplenomegaly, was significantly higher in patients with autoimmunity (<em>p=0.004</em>). Syndromic CID patients with autoimmunity had significantly lower IgG levels. Hematologic autoimmunity mainly immune thrombocytopenic purpura was the most frequent autoimmunity among major groups of <em>ATM</em>, <em>STAT3,</em> <em>DNMT3B/ ZBTB24,</em> and <em>WAS</em> mutations, however <em>ATM-</em>mutated patients present more diversified involved organs including rheumatologic, gastrointestinal and dermatologic autoimmunity.</p> <p><strong><em>Conclusion</em></strong><strong>:</strong> About 18% of patients with monogenic syndromic CIDs developed autoimmunity, mainly in the form of hematological immune diseases. Autoimmunity could be an early-onset involvement with a potential diagnostic impact on suspicious cases of syndromic CIDs.</p>
IL-2 in Refractory Autoimmune Encephalitis
ClinicalTrials.gov study NCT02714959. IPD Sharing: Not stated. Countries: 0. Publications: 6.
Diabetes Autoimmunity Withdrawn In New Onset and In Established Patients
ClinicalTrials.gov study NCT03895437. IPD Sharing: NO. Countries: 1. Publications: 0.
Evaluating Sirolimus to Treat Autoimmune Blistering Dermatosis Pemphigus
ClinicalTrials.gov study NCT01313923. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Presence of Circulating Cluster of Differentiation 4 Positive 28 Null T Helper Lymphocytes(CD4+CD28-) in Patients With Autoimmune Hemolytic Anemia.
ClinicalTrials.gov study NCT05711264. IPD Sharing: Not stated. Countries: 0. Publications: 6.
Study of Ianalumab in Adults With Primary Immune Thrombocytopenia (ITP) and Warm-antibody Autoimmune Hemolytic Anemia (wAIHA) Who Have Previously Benefited From Ianalumab
ClinicalTrials.gov study NCT07039422. IPD Sharing: YES. Countries: 1. Publications: 0.
Steroid Therapy in Autoimmune Premature Ovarian Failure
ClinicalTrials.gov study NCT00001306. IPD Sharing: Not stated. Countries: 1. Publications: 3.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.