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3,441 results for “Immune cells”
Integration of single-cell RNA-sequencing data across tissues and cancer types towards immune cell characterization
<p>To better understand dendritic cell states and subtypes, we collected individual single-cell RNAseq datasets from various studies and further integrated, batch corrected, and reprocessed the data using Besca (https://github.com/bedapub/besca).</p> <p>The following files are included:<br> 1) study_table_integrated_DCs.xlsx - contains a list of studies from where the datasets were gathered.<br> 2) int_dcs.raw.h5ad - An anndata object file containing the combined raw single-cell counts for DCs from individual studies. The datasets were joined based on the union of variables.<br> 3) intersection_genes_integrated_dcs.tsv - List of genes if the datasets were joined based on the intersection of variables. These variables were used in the subsequent analyses.</p> <p>4) int_dcs.annotated.h5ad - An anndata object file containing single-cell logarithmized counts for DCs data that have been integrated and reprocessed. The rows of the file contain cells, and the columns contain highly variable genes. A sparse matrix containing the logarithmized counts from all the genes (from the intersection genes integrated dcs.tsv file) can also be found (adata.raw.X) in the object. In the observations, cell-type annotation is available at three different hierarchal levels.<br> <br> This data was further used to produce results for the publication (https://jitc.bmj.com/content/10/6/e004268) on the effects of Toll-like receptor 8 agonists on conventional DCs.</p>
Proteomic and Metabolomic Profiling of Plasma Predict Immune-related Adverse Events in Older Patients with Advanced Non-small Cell Lung Cancer
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scTransformers - Dataset : Cross Tissue Immune Cells
<p>The annotation of cell types on single cell RNA-seq data is a complex, uncertain and time-consuming task, requiring several methods and tools to be able to annotate cells appropriately and efficiently. To overcome these problems and uncertainties, numerous tools and scientific articles have emerged over the years. The rise of artificial intelligence in our lives (notably through chatGPT), has also imposed itself on the scientific world, bringing novelty and innovation to existing techniques and tools. These tools need to be tested and studied to verify their effectiveness. In this project, two cell annotation tools in single cell RNA-seq named scBERT and scGPT are of interest to CB2M because of their ability to resolve and avoid the uncertainties and problems mentioned above. We study here, through various analyses, including cross-validation and the use of multiple qualitative and numerical indicators, that cell annotation by those tools are effective for annotating cells from scRNA-seq.</p> <p>Provided files :</p> <ul> <li>Human_Thymus_Development_Atlas_reference.tar.gz : Cell atlas of human thymic development : 15 embryonic and fetal thymuses covering stages of thymic development from 7 post-conceptional weeks (PCW) to 17 PCW, and 9 postnatal thymuses from human pediatric and adult samples. It contains 255,901 cells, 32,922 genes and 33 different cell types.</li> <li>Human_Thymus_Development_Atlas_output.tar.gz : All analysis output files</li> <li>Human_Thymus_Development_Atlas_container.tar.gz : Docker image and Singularity mages used for the analysis</li> </ul> <p>See https://github.com/CIML-bioinformatic/CB2M_scTransformers for more details.</p>
scTransformers - Dataset : Cross Tissue Immune Cells
<p>The annotation of cell types on single cell RNA-seq data is a complex, uncertain and time-consuming task, requiring several methods and tools to be able to annotate cells appropriately and efficiently. To overcome these problems and uncertainties, numerous tools and scientific articles have emerged over the years. The rise of artificial intelligence in our lives (notably through chatGPT), has also imposed itself on the scientific world, bringing novelty and innovation to existing techniques and tools. These tools need to be tested and studied to verify their effectiveness. In this project, two cell annotation tools in single cell RNA-seq named scBERT and scGPT are of interest to CB2M because of their ability to resolve and avoid the uncertainties and problems mentioned above. We study here, through various analyses, including cross-validation and the use of multiple qualitative and numerical indicators, that cell annotation by those tools are effective for annotating cells from scRNA-seq.</p> <p>Provided files:</p> <ul> <li>cross_tissue_immune_cell_reference.tar.gz : Cell atlas across tissue in human immune system : Immune compartment of 15 tissues from six deceased adult donors. It contains 329,762 cells, 36,398 genes and 35 different cell types.</li> <li>cross_tissue_immune_cell_output.tar.gz : All analysis output files</li> <li>cross_tissue_immune_cell_container.tar.gz : Docker image and Singularity mages used for the analysis</li> </ul> <p>See https://github.com/CIML-bioinformatic/CB2M_scTransformers for more details</p>
Distant metastases of breast cancer resemble primary tumors in tumor cell composition but differ in immune cell phenotypes
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Single cell data from Imaging Mass Cytometry of mouse lung tumours treated with KRAS-G12C and immune checkpoint inhibitors (Dataset 3)
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ASO-mediated knockdown of GPNMB in mutant-GRN and Grn-deficient peripheral myeloid cells disrupts lysosomal function and immune responses
<p><strong>Background: </strong>Increases in GPNMB are detectable in FTD-<em>GRN</em> cerebrospinal fluid (CSF) and post-mortem brain, and brains of aged <em>Grn</em>-deficient mice. Although no upregulation of GPNMB is observed in the brains of young <em>Grn</em>-deficient mice, peripheral immune cells of these mice do exhibit this increase in GPNMB. Importantly, the functional significance of GPNMB upregulation in progranulin-deficient states is currently unknown. Given that GPNMB has been discussed as a potential therapeutic target in <em>GRN</em>-mediated neurodegeneration, it is vital for the field to determine what the normal function of GPNMB is in the immune system, and whether targeting GPNMB will elicit beneficial or deleterious effects.</p> <p><strong>Methods: </strong>The effects of GPNMB knock-down via antisense oligonucleotide (ASO) were assessed in peripheral blood mononuclear cells (PBMCs) from 25 neurologically healthy controls (NHCs) and age- and sex-matched FTD-<em>GRN </em>patients, as well as peritoneal macrophages (pMacs) from progranulin-deficient (<em>Grn</em><sup>-/-</sup>) and B6 mice. Lysosomal function, antigen presentation and MHC-II processing and recycling were assessed, as well as cytokine release and transcription.</p> <p><strong>Results: </strong>We demonstrate here that ASO-mediated knockdown of GPNMB increases lysosomal burden and cytokine secretion in FTD-GRN carrier and neurologically healthy controls (NHCs) monocytes. <span>ASO-mediated knockdown of GPNMB in <em>Grn</em>-deficient macrophages decreased lysosomal pan-cathepsin activity and protein degradation. In addition, </span>ASO-mediated knockdown of GPNMB increased MHC-II surface expression, which was driven by decreased MHC-II uptake and recycling, in macrophages from <em>Grn</em>-deficient females. Finally, ASO-mediated knockdown of GPNMB dysregulated IFN<span><span><span>g</span></span>-stimulated cytokine transcription and secretion by mouse macrophages due to the absence of regulatory actions of the GPNMB extracellular fragment (ECF). </span></p> <p><strong>Conclusions: </strong><span>Our data herein reveals that </span>GPNMB has a regulatory effect on multiple immune effector functions, including capping inflammation and immune responses in myeloid cells via secretion of its ECF. Therefore, in progranulin-deficient states, the drastic upregulation in GPNMB transcript and protein may represent a compensatory mechanism to preserve lysosomal function in myeloid cells. These novel findings indicate that targeted depletion in FTD-<em>GRN</em> would not be a rational therapeutic strategy because it is likely to dysregulate important immune cell effector functions.</p>
Source data sets_Figure 1, 2, 6_Salmonella cancer therapy metabolically disrupts tumours at the collateral cost of T cell immunity
<p>Flow cytometry data files associated with Copland <em>et al., </em><strong><em><span>Salmonella </span></em></strong><strong><span>cancer therapy metabolically disrupts tumours at the collateral cost of T cell immunity.</span></strong></p> <p><span>Data associated to Figures 1, 2 and 6. <br></span></p>
Single-cell atlas of circulating immune cells over the first two months of age in extremely premature infants
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Supplemental tables for: A periventricular gradient of innate immune cell activation in Multiple Sclerosis
<p><span><span><span><span><span><span><span><span><span><span><span><b>Objectives:</b> To explore <i>in-vivo</i> innate immune cell activation as a function of the distance from ventricular CSF in patients with Multiple Sclerosis (MS) using [18F]-DPA714 PET, and to investigate its relationship with periventricular microstructural damage, evaluated by magnetization transfer ratio (MTR), and with trajectories of disability worsening.</span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Methods: </b>Thirty-seven MS patients and nineteen healthy controls underwent MRI and [18F]-DPA714 TSPO dynamic PET, from which individual maps of voxels characterized by innate immune cell activation (DPA+) were generated. White matter (WM) was divided in 3mm-thick concentric rings radiating from the ventricular surface toward the cortex, and the percentage of DPA+ voxels and mean MTR were extracted from each ring. Two-year trajectories of disability worsening were collected to identify patients with and without recent disability worsening.</span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Results: </b>The percentage of DPA+ voxels was higher in patients compared to controls in the periventricular WM (<span><span>p=6.10e-6</span></span>), and declined with increasing distance from ventricular surface, with a steeper gradient in patients compared to controls (<span><span>p=0.001</span></span>). This gradient was found both in periventricular lesions and normal-appearing WM. In the total WM, it correlated with a gradient of microstructural tissue damage measured by MTR (<span><span>r<sub>s</sub>=-0.65, p=1.0e-3</span></span>). When compared to clinically stable patients, patients with disability worsening were characterized <span><span>by a higher percentage of DPA+ voxels </span></span>in the periventricular normal-appearing WM (<span><span>p=0.025</span></span>).</span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><b>Conclusions: </b>Our results demonstrate that in MS the innate immune cell activation predominates in periventricular regions and associates with microstructural damage and disability worsening. This could result from the diffusion of pro-inflammatory CSF-derived factors into surrounding tissues.</span></span></span></span></span></span></span></span></span></span></span></p>
Code and Data to recreate figures from: Activation of immune receptor Rx1 triggers distinct immune-responses culminating in cell death after four hours.
<p>Code and Data to recreate figures from: Activation of immune receptor Rx1 triggers distinct immune-responses culminating in cell death after four hours.</p> <p><a href="https://doi.org/10.1111/mpp.12776">https://doi.org/10.1111/mpp.12776</a></p> <p> </p> <p>These files are also on Github:</p> <p>https://github.com/MolPlantPathology/PMID-30537296-</p>
Single-cell heterogeneity of EGFR and CKD4 co-amplification is linked to immune infiltration in glioblastoma
<p>This upload contains RDS objects of preprocessed publicly available scRNAseq data, required to run scRNAseq analyses in the manuscript "Single cell heterogeneity of EGFR and CDK4 co-amplification is linked to immune infiltration in glioblastoma". The corresponding GitHub repo <a href="https://github.com/Michorlab/GBM_OR_immune">https://github.com/Michorlab/GBM_OR_immune</a> contains code to analyze the data here, as well as plots and tables generated on the basis of this data.</p>
Genetic variation in cis-regulatory domains suggests cell type-specific regulatory mechanisms in immunity
<p>1- workflow for data analysis and figures generation</p>
Immune Checkpoint Inhibitor, Nivolumab, Combined with Chemotherapy Improved the Survival of Unresectable Ad-vanced and Metastatic Esophageal Squamous Cell Carcinoma: a real world experience
<p><strong>Figure S1 the detail of treatments.</strong> Blue arrow means this patient was still alive at the latest date of follow up. Hollow circle means this patient die. The others were lose follow up at the latest date of follow up.</p> <p><strong>Figure S2 progression free survival (PFS) of patients received immunotherapy, including 5 nivolumab and chemotherapy and 1 dual immune check point inhibitor, on different PD-L1 tumor cells (TC) expression.</strong> (A) divided by PD-L1 TC <1% or ≧1%. (B)divided by PD-L1 TC <10% or ≧10%.</p>
Data for: Low protease activity in B cell follicles promotes retention of intact antigens after immunization
<p>The structural integrity of vaccine antigens is critical to the generation of protective antibody responses, but the impact of protease activity on vaccination in vivo is poorly understood. We characterized protease activity in lymph nodes and found that antigens were rapidly degraded in the subcapsular sinus, paracortex, and interfollicular regions, whereas low protease activity and antigen degradation rates were detected in the vicinity of follicular dendritic cells (FDCs). Correlated with these findings, immunization regimens designed to target antigen to FDCs led to germinal centers dominantly targeting intact antigen, whereas traditional immunizations led to much weaker responses that equally targeted the intact immunogen and antigen breakdown products. Thus, spatially compartmentalized antigen proteolysis affects humoral immunity and can be exploited.</p>
Interaction of Bacteria, Immune Cells, and Surface Topography in Periprosthetic Joint Infections
<p>This record contains raw data related to article “Interaction of Bacteria, Immune Cells, and Surface Topography in Periprosthetic Joint Infections”</p>
Benchmark datasets for "Detecting T-cell expansion and quantifying clone survival from deep profiling of immune repertoires"
<p>T-cell receptor repertoire sequencing datasets describing time courses obtained for vaccination, normal aging and blood transplant cases. Datasets reported here were previously published (except for Tem/Tcm data), this is just a compendium of selected samples that is properly pre-processed and formatted.</p>
CD4 T cell receptor hierarchies are stable and independent of HIV-mediated dysregulation of immune homeostasis
<p>LT-ART and A5248 folders contain preprocessed CyTOF files (FCS format) from a 31-marker mass cytometry panel to examine all major PBMC lineages and specifically CD4 and CD8 T cell memory dynamics in people with HIV (PWH) who are durably ART suppressed for an average of 6.7 years (LT-ART, n = 10) and PWH in the first 500 days following ART initiation (A5248, n = 10). The panel also includes markers of activation (HLA-DR, CD38, CCR5), activation/exhaustion (PD-1), proliferation (Ki67), survival (Bcl-2) and long-lived memory (CD127).</p> <p>Preprocessed annotated data objects (A5248_subsample.h5ad, LT-ART_subsample.h5ad) for unsupervised analysis can be accessed using the 'read_h5ad' function in Scanpy.</p> <p>CD4_MSI and CD8_MSI folders contain the MSI data for the Gamma fixed-effects regression models. </p> <p>All source code for reproduction of the results can be found in the GitHub repository: <a href="https://github.com/glab-hiv/immune-recovery">https://github.com/glab-hiv/immune-recovery</a></p>
TSPO acts as an immune resistance gene involved in the T cell mediated immune control of glioblastoma
<p>Glioblastoma (GB) IDH-wildtype is the most malignant primary brain tumor. It is particularly resistant to current immunotherapies. Translocator protein 18 kDa (TSPO) is upregulated in GB and correlates with malignancy and poor prognosis, but also with increased immune infiltration. Here, we studied the role of TSPO in the regulation of immune resistance of human GB cells. The role of TSPO in tumor immune resistance was experimentally determined in primary brain tumor initiating cells (BTICs) and cell lines through genetic manipulation of TSPO expression and subsequent cocultures with antigen specific cytotoxic T cells and autologous tumor-infiltrating T cells. Death inducing intrinsic and extrinsic apoptotic pathways affected by TSPO were investigated. TSPO-regulated genes mediating apoptosis resistance in BTICs were identified through gene expression analysis and subsequent functional analyses. TSPO transcription in primary GB cells correlated with CD8<sup>+</sup> T cell infiltration, cytotoxic activity of T cell infiltrate, expression of TNFR and IFNGR and with the activity of their downstream signalling pathways, as well as with the expression of TRAIL receptors. Coculture of BTICs with tumor reactive cytotoxic T cells or with T cell-derived factors induced TSPO up-regulation through T cell derived TNFα and IFNγ. Silencing of TSPO sensitized BTICs against T cell-mediated cytotoxicity. TSPO selectively protected BTICs against TRAIL-induced apoptosis by regulating apoptosis pathways. TSPO also regulated the expression of multiple genes associated with resistance against apoptosis. We conclude that TSPO expression in GB is induced through T cell-derived cytokines TNFα and IFNγ and that TSPO expression protects GB cells against cytotoxic T cell attack through TRAIL. Our data thereby provide an indication that therapeutic targeting of TSPO may be a suitable approach to sensitize GB to immune cell-mediated cytotoxicity by circumventing tumor intrinsic TRAIL resistance.</p>
IL-18 couples innate and adaptive immune cell activation in acute multisystem inflammatory syndrome in children (MIS-C)
<p>This repository contains the scRNA-Seq data (including TCR-Seq and BCR-Seq data) set used in the manuscript titled "IL-18 couples innate and adaptive immune cell activation in acute multisystem inflammatory syndrome in children (MIS-C)". This dataset is generated from 10x cell ranger software. In the study, we have 10 PBMC samples, from 5 MIS-C children at paired time points. T1 stands for admission time and T3 follow-up time, about 1 month post hospital discharge. </p>
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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.