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1,355 results for “Autoimmunity”
Flow cytometry of mesenteric lymph nodes, small and large intestinal lamina propria, and spinal cord cells from fibre-rich and fiber-free diet-fed gnotobiotic mice at baseline and after experimental autoimmune encephalomyelitis (EAE) induction
<p>We perform profiling of different immune cell populations in the small (SILP) and large intestine lamina propria (CLP), mesenteric lymph nodes (MLN) and spinal cords (SC). We are specifically interested to evaluate the impact of dietary fiber deprivation followed by mucus erosion on the immune cell profiles of T helper cells (Th cells, T cell population) of gnotobiotic mice fed a fiber-rich (FR) or fiber-free (FF) diet. This dataset aims to assess the impact of microbiome and diet on disease course in a mouse model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE) via T cell populations. Mice are either germ-free or colonized by intragastric gavage with a defined variation of a 14-member synthetic human gut microbiome (doi: 10.1016/j.cell.2016.10.043 and 10.1016/j.xpro.2021.100607): SM01 (Akkermansia muciniphila monocolonisation), SM03 (Bacteroides caccae, Bacteroides thetaiotaomicron, Barnesiella intestinihominis), SM04 (B. caccae, B. thetaiotaomicron, B. intestinihominis, A. muciniphila), SM12 (full community except mucin-specialists B. intestinihominis and A. muciniphila), SM13 (full community except mucin specialist A. muciniphila), or SM14 (full community: Roseburia intestinalis, Faecalibacterium prausnitzii, Marvinbryantia formatexigens, Collinsella aerofaciens, Desulfovibrio piger, B. caccae, B. thetaiotaomicron, Bacteroides ovatus, Bacteroides uniformis, B. intestinihominis, Eubacterium rectale, Clostridium symbiosum, Escherichia coli, and A. muciniphila). At age 5 to 8 weeks, mice were colonized with SM combinations while fed an FR diet. Mice were either maintained on an FR diet or switched to an FF diet at 5 days after initial colonization, until the end of experiment. Baseline samples were collected 20 days following the diet switch. Otherwise, EAE induction was performed 15 days after the diet switch and samples were collected 30 days after the induction.</p>
Dataset of Molecular Dynamics Simulations for the Upregulated Biomarker PSMB8: 3UNF and its G210V Mutant in Experimental Autoimmune Encephalomyelitis
<p>This dataset contains molecular dynamics simulations data generated using GROMACS for the upregulated biomarker 3UNF and its G210V mutant in the context of Experimental Autoimmune Encephalomyelitis (EAE). EAE is a widely studied animal model for multiple sclerosis, and investigating the behavior of biomarkers in this model is crucial for understanding disease progression and potential therapeutic interventions.</p> <p>The dataset includes trajectory files, coordinate files, and relevant parameters used in the simulations. These simulations provide valuable insights into the structural dynamics, conformational changes, and interactions of the PSMB8 biomarker 3UNF and its G210V mutant within the EAE system. The data offers researchers an opportunity to analyze and explore the behavior of these biomarkers at the atomic level, aiding in the identification of potential binding partners, functional sites, and mechanisms associated with disease progression.</p> <p>By sharing this dataset, we aim to contribute to the scientific community by providing a valuable resource for further analysis, validation, and comparison of the molecular behavior of the upregulated biomarker 3UNF and its G210V mutant in Experimental Autoimmune Encephalomyelitis.</p>
KCNA2 IgG Autoimmunity In Neuropsychiatric Diseases
<p>One patient of the cohort (#25) received a temporal lobe biopsy to rule out a malignant disease. Histological and immunohistochemical images of diagnostic sections are shown. From these images regions of interest are shown in Figure 2.</p>
Natural Killer cells demonstrate distinct eQTL and transcriptome-wide disease associations, highlighting their role in autoimmunity.
<p><strong>Abstract</strong> </p> <p>Natural Killer (NK) cells are innate lymphocytes with central roles in immunosurveillance and are implicated in autoimmune pathogenesis. The degree to which regulatory variants affect NK gene expression is poorly understood. We performed expression quantitative trait locus (eQTL) mapping of negatively selected NK cells from a population of healthy Europeans (n=245). We find a significant subset of genes demonstrate eQTL specific to NK cells and these are highly informative of human disease, in particular autoimmunity. An NK cell transcriptome-wide association study (TWAS) across five common autoimmune diseases identified further novel associations at 27 genes. In addition to these <em>cis</em> observations, we find novel master-regulatory regions impacting expression of <em>trans</em> gene networks at regions including 19q13.4, the Killer cell Immunoglobulin-like Receptor (KIR) Region, <em>GNLY</em>, <em>MC1R</em> and<em> UVSSA</em>. Our findings provide new insights into the unique biology of NK cells, demonstrating markedly different eQTL from other immune cells, with implications for disease mechanisms.</p> <p><strong>Preprint</strong></p> <p>https://www.biorxiv.org/content/10.1101/2021.05.10.443088v1</p> <p><strong>Dataset</strong></p> <p>nk_raw_for_zenodo.txt: Matrix of raw gene expression at 47,209 probes in primary human NK cells from 245 healthy individuals of European ancestry. Gene expression is quantified using the Illumina HumanHT-12 v4 BeadChip gene expression array platform. Column names represent Array Address ID for each probe, and row names represent pseudonymised sample identifiers, which can be matched to sample genotypes. Sample genotypes are available at the European Genome-Phenome Archive with accession ID EGAS00000000109).</p> <p>probes_passing_QC.txt: List of probes passing quality control; probe sequences mapping to a unique genomic locus, and probe sequences not containing common genomic variation (minor allele frequency >1%), n=29,002. Column names are Array Address ID (probeID), Ensembl ID (ensembl), Gene ID (gene), and Illumina probe ID (ilmn). </p>
Basket Study to Assess Efficacy, Safety and PK of Iptacopan (LNP023) in Autoimmune Benign Hematological Disorders
ClinicalTrials.gov study NCT05086744. IPD Sharing: YES. Countries: 6. Publications: 1.
Gut Microbiota from Multiple Sclerosis patients triggers spontaneous autoimmune encephalomyelitis in mice --shotgun data--
Open the record for dataset details and reuse information.
Gut Microbiota from Multiple Sclerosis patients triggers spontaneous autoimmune encephalomyelitis in mice --16S data--
Open the record for dataset details and reuse information.
Dataset related to article "IL1R8 Deficiency Drives Autoimmunity-Associated Lymphoma Development."
<p>Chronic inflammation, including that driven by autoimmunity, is associated with the development of B-cell lymphomas. IL1R8 is a regulatory receptor belonging to the IL1R family, which negatively regulates NF-κB activation following stimulation of IL1R or Toll-like receptor family members. IL1R8 deficiency is associated with the development of severe autoimmune lupus-like disease in <em>lpr</em> mice. We herein investigated whether concomitant exacerbated inflammation and autoimmunity caused by the deficiency of IL1R8 could recapitulate autoimmunity-associated lymphomagenesis. We thus monitored B-cell lymphoma development during the aging of IL1R8-deficient <em>lpr</em> mice, observing an increased lymphoid cell expansion that evolved to diffuse large B-cell lymphoma (DLBCL). Molecular and gene-expression analyses showed that the NF-κB pathway was constitutively activated in <em>Il1r8</em> <sup>-/-</sup>/<em>lpr</em> B splenocytes. In human DLBCL, <em>IL1R8</em> had reduced expression compared with normal B cells, and higher <em>IL1R8</em> expression was associated with a better outcome. Thus, <em>IL1R8</em> silencing is associated with increased lymphoproliferation and transformation in the pathogenesis of B-cell lymphomas associated with autoimmunity.</p>
Analysis of gene expression in autoimmune and autoinflammatory diseases using GSEA
<p>This dataset contains the results of gene set enrichment analysis (GSEA) of gene expression in the studied diseases. The archive is organized in folders according the GEO accessions for the raw data (see table 1 of the main article). If multiple diseases were studied within one GEO data series, GSEA was performed for each disease separately. Healthy subject data included in each data series were used as reference. </p> <p>For example <strong><em>"GSE3365.IBD"</em></strong> folder contains GSEA for Crohn's disease (CD) and ulcerative colitis (US). The <em><strong>"results"</strong></em> folder in <em><strong>"GSE3365.IBD"</strong></em> contains two subfolders <strong><em>"GSE3365CDvcHC"</em></strong> and <em><strong>"GSE3365UCvcHC"</strong></em>, respectively. The results can be browsed with <em><strong>"index.html"</strong></em> files located in each subfolder. </p>
Transcobalamin receptor antibodies in autoimmune vitamin B12 central deficiency
<p>Vitamin B12 is critical for hematopoiesis and myelination. Deficiency can cause neurologic deficits including loss of coordination and cognitive decline. However, diagnosis relies on vitamin B12 measurement in the blood which may not accurately reflect levels in the brain. Using programmable phage display, we identified an autoantibody targeting the transcobalamin receptor (CD320) in a patient with progressive tremor, ataxia, and scanning speech. Anti-CD320 impaired cellular uptake of cobalamin (B12) <em>in vitro</em>. Despite normal serum levels, B12 was nearly undetectable in her cerebrospinal fluid (CSF). Immunosuppressive treatment and high-dose systemic B12 supplementation were associated with increased CSF B12 levels and clinical improvement. Optofluidic screening enabled rapid isolation of a patient-derived monoclonal antibody that impaired B12 transport across an <em>in vitro</em> model of the blood-brain barrier. Autoantibodies targeting the same epitope of CD320 were identified in 7 other patients with neurologic deficits of unknown etiology, in 6% of healthy controls, and in 21.4% of a neuropsychiatric lupus cohort. In 132 paired serum and CSF samples, detection of anti-CD320 in the blood predicted B12 deficiency in the brain. However, these individuals did not display any hematologic signs of B12 deficiency despite systemic CD320 impairment. Using a genome-wide CRISPR screen, we discovered that the LDL receptor serves as an alternative B12 uptake pathway in hematopoietic cells. These findings dissect the tissue-specificity of B12 transport and elucidate an autoimmune neurologic condition that may be amenable to immunomodulatory treatment and nutritional supplementation.</p>
Autoimmunity-associated allele of tyrosine phosphatase gene PTPN22 enhances anti-viral immunity
<p>The 1858C>T allele of the tyrosine phosphatase <em>PTPN22</em> is present in 5-10% of the North American population and is strongly associated with numerous autoimmune diseases. Although research has been done to define how this allele potentiates autoimmunity, the influence <em>PTPN22</em> and its pro-autoimmune allele have in anti-viral immunity remains poorly defined. Here, we use single-cell RNA-sequencing and functional studies to interrogate the impact of this pro-autoimmune allele on anti-viral immunity during Lymphocytic Choriomeningitis Virus clone 13 (LCMV-cl13) infection. Mice homozygous for this allele (PEP-619WW) clear the LCMV-cl13 virus whereas wildtype (PEP-WT) mice cannot. This is associated with enhanced anti-viral CD4 T cell responses and a more immunostimulatory CD8a<sup>-</sup> cDC phenotype. Adoptive transfer studies demonstrated that PEP-619WW enhanced anti-viral CD4 T cell function through virus-specific CD4 T cell-intrinsic and extrinsic mechanisms. Taken together, our data show that the pro-autoimmune allele of <em>Ptpn22</em> drives a beneficial anti-viral immune response thereby preventing what is normally a chronic virus infection.</p>
Normalized linear counts from NanoString autoimmune profiling panel and summary of statistical analyses
<p>Though dependent on genetic anomalies, clinical manifestations of the human autoimmune disease systemic lupus erythematosus (lupus) can be triggered by environmental exposures including inhalation toxicants such as crystalline silica dust (cSiO<sub>2</sub>), tobacco smoke, and ambient air particles. Prednisone, a glucocorticoid (GC), is a keystone therapy for managing lupus flaring and progression, however, long-term use is associated with many adverse side effects. Here, we characterized the dose-dependent immunomodulation and toxicity of prednisone in a preclinical model that emulates onset and progression of cSiO<sub>2</sub>-triggered lupus. Two cohorts of 6-wk-old female NZBWF1 mice were fed either control AIN-93G diet or one of three AIN-93G diets containing prednisone at 5, 15, or 50 mg/kg diet which span human equivalent oral doses (HED) currently considered to be low (PL; 5 mg/d HED), moderate (PM; 14 mg/d HED), or high (PH; 46 mg/d HED), respectively. At 8 wk of age, mice were intranasally instilled with either saline vehicle or 1 mg cSiO<sub>2</sub> once weekly for 4 wk. The experimental plan was to 1) terminate one cohort of mice (n=8/group) 14 wk after the last cSiO<sub>2</sub> instillation for pathology and autoimmunity assessment and 2) to maintain a second cohort (n=9/group) to monitor glomerulonephritis development and survival. Mean blood concentrations of prednisone's chief active metabolite, prednisolone, in mice fed PL, PM, and PH diets were 27, 105, 151 ng/ml, respectively, which are consistent with levels observed in human blood ≤ 12 h after single bolus treatments with equivalent prednisone doses. Results from the first cohort revealed that consumption of PM but not PL diet significantly reduced cSiO<sub>2</sub>-induced pulmonary ectopic lymphoid structure formation, nuclear-specific AAb production, and inflammation/autoimmune gene expression in the lung, splenomegaly, and glomerulonephritis in the kidney. Relative to GC-associated toxicity, PM but not PL diet elicited muscle wasting, but these diets did not affect bone density or cause glucosuria. Importantly, neither PM nor PL diet influenced latency of cSiO<sub>2</sub>-accelerated death. PH-fed mice in both cohorts displayed robust GC-associated toxicity including body weight loss, reduced muscle mass, and hyperglycemia 7 wk after the final cSiO<sub>2</sub> instillation requiring their early removal from the study. Taken together, our results demonstrate that while moderate doses of prednisone can reduce certain pathological endpoints of cSiO<sub>2</sub>-induced autoimmunity in lupus-prone mice, these ameliorative effects come with unwanted GC toxicity and, crucially, none of these three doses extended survival time.</p>
Broccoli sprout beverage is safe for thyroid hormonal and autoimmune status: Results of a 12-week randomized trial.
<p>The .csv file contains all the primary data for publication: <br> Chartoumpekis DV, Ziros PG, Chen JG, Groopman JD, Kensler TW, Sykiotis GP.<br> Broccoli sprout beverage is safe for thyroid hormonal and autoimmune status: Results of a 12-week randomized trial.<br> Food Chem Toxicol. 2019 Feb 5;126:1-6.<br> [Epub ahead of print] PubMed PMID: 30735751<br> doi: 10.1016/j.fct.2019.02.004.</p> <p>These data are used in all figures of the paper (Figure 1 and Figure 2).</p> <p>The data are tabular. The headers are the following:</p> <p>sample ID: It comprises 4 digits. The first 3 digits are the unique identifier of the subject in the trial, e.g., "613".<br> The last digit indicates whether the sample was collected at the start of the trial "0", or at the end of the trial "1".<br> E.g., "6130" is the sample collected from participant 613 at the beginning of the trial,<br> and 6131 is the sample collected from the same participant at the end of the trial.</p> <p>Autoimmunity: "0" means that both anti-TG and anti-TPO antibodies were within the reference range.<br> "1" means that either anti-TG, or anti-TPO antibodies, or both, were above the reference range.</p> <p>anti-TG (IU/ml): antibodies against thyroglobuline. The units are given in the parenthesis.</p> <p>anti-TPO (IU/ml): antibodies against thyropreoxidase. The units are given in the parenthesis.</p> <p>Treatment: "1"=placebo and "2"=broccoli sprouts extract beverage.</p> <p>Gender: "F" for female and "M" for male. Data from males were not included in the analyses.</p> <p>Age: In years.</p> <p><br> For any questions, contact: gerasimos.sykiotis@chuv.ch</p>
Data from: Docosahexaenoic acid intake suppresses acute silica-induced inflammation, autoantibody production, and autoimmune-related gene expression in lupus-prone mice
<p class="MsoNormal">Short-term repeated intranasal exposure crystalline silica (cSiO<sub>2</sub>), a known human autoimmune trigger, induces uncontrolled inflammation, upregulated IFN-stimulated gene expression, diverse autoantibody production, and glomerulonephritis in lupus-prone female NZBWF1 mice. Dietary supplementation with the omega-3 fatty acid docosahexaenoic acid (DHA) prevents subchronic cSiO<sub>2</sub> triggering of these lupus hallmarks. To understand how this intervention impacts acute effects of cSiO<sub>2</sub>, we fed NZBWF1 mice control (CON) or DHA-containing diet, subjected them to a single acute intranasal instillation of 2.5 mg cSiO<sub>2</sub>, then compared pulmonary inflammatory/autoimmune responses and autoimmune-related gene expression in experimental cohorts terminated at 7 and 28 d post-instillation (PI). Acute cSiO<sub>2 </sub>exposure of CON-fed mice elicited decreased macrophage and increased neutrophil numbers at 7 d PI, whereas at 28 d PI, CON-fed mice treated with particle displayed elevated total cell, macrophage, neutrophil, and lymphocyte counts. In contrast, DHA-fed mice treated with cSiO<sub>2</sub> exhibited less macrophage loss at 7 d PI and reduced total cell, macrophage, and lymphocyte accumulation at 28 d PI. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) of lung sections suggested that cSiO<sub>2</sub> induced more robust cell death at 7 d PI in CON-fed than DHA-fed mice. Targeted multiplex ELISA of lung extracts showed that at 28 d PI, cSiO<sub>2</sub> induced higher concentrations of inflammation-associated cytokines (IL-1α, IL-6, and GM-CSF) and IFN-stimulated chemokines (CCL2, CCL3, CXCL10) in the CON-fed cohort than in the DHA-fed cohort. Autoantigen protein microarray of BALF collected at 28 d PI indicated that cSiO<sub>2</sub> induced higher autoantibody responses for representative nuclear, ribosomal, mitochondrial, and complement proteins in CON-fed mice than DHA-fed mice. Gene expression analyses with NanoString Autoimmune Gene Expression assay revealed greater cSiO<sub>2</sub>-triggered upregulation of genes associated with TLR activation, DNA signaling, proinflammatory cytokines, chemokines, type 1 and 2 IFN response signatures, lymphocyte trafficking, MHC class 1 antigen presentation, B and T cell activation at 7 and 28 d PI in CON-fed mice than those fed DHA. Ingenuity Pathway Analysis (IPA) further demonstrated that DHA supplementation quelled cSiO<sub>2</sub>-induced responses top upstream regulators of proinflammatory and IFN-regulated gene networks to observed in CON-fed mice. Altogether, this short-term model illustrated that DHA suppression of aberrant acute cSiO<sub>2</sub>-induced inflammation is linked to altered regulation of autoimmune-related gene expression in lupus-prone mice.</p>
AutoCore: network-based definition of the core module of human autoimmunity and autoinflammation
<p><span>Although research on rare autoimmune and autoinflammatory diseases has enabled definition of non-redundant regulators of homeostasis in human immunity, due to the single gene-single disease nature of many of these diseases, contributing factors were mostly unveiled in sequential and non-coordinated individual studies. </span><span>Here, we used a network-based approach for integrating a set of 186 inborn errors of immunity with predominant autoimmunity/autoinflammation into a comprehensive map of human immune dysregulation which we termed "AutoCore". The AutoCore is located centrally within the interactome of all protein-protein interactions, connecting and pinpointing multi-disease markers for a range of common, polygenic autoimmune/autoinflammatory diseases. The AutoCore can be subdivided into 19 endotypes that correspond to molecularly and phenotypically cohesive disease subgroups, providing a molecular mechanism-based disease classification and rationale towards systematic targeting for therapeutic purposes. Our study provides a proof-of-concept for using network-based methods to systematically investigate the molecular relationships between individual rare diseases and address a range of conceptual, diagnostic, and therapeutic challenges.</span></p>
sPIF CLINICAL STUDY PROTOCOL IN AUTOIMMUNE HEPATITIS
ClinicalTrials.gov study NCT02239562. IPD Sharing: NO. Countries: 1. Publications: 2.
Efficacy and Safety of Inhaled Molgramostim (rhGM-CSF) in Autoimmune Pulmonary Alveolar Proteinosis
ClinicalTrials.gov study NCT02702180. IPD Sharing: NO. Countries: 18. Publications: 1.
Supplementation With B. Infantis for Mitigation of Type 1 Diabetes Autoimmunity
ClinicalTrials.gov study NCT04769037. IPD Sharing: NO. Countries: 5. Publications: 1.
Autoimmune and Autoinflammatory Genetics Study
ClinicalTrials.gov study NCT06004349. IPD Sharing: YES. Countries: 1. Publications: 2.
Sirolimus Injections for Autoimmune Scleritis
ClinicalTrials.gov study NCT01517074. IPD Sharing: Not stated. Countries: 1. Publications: 4.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.