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12,799 results for “Immunization”
Additional data repository for the study of Alpha-synuclein aggregates trigger anti-viral immune pathways and RNA editing in human astrocytes
<p>Zip file 1: astrocytes calcium data measured using Fura 2</p> <p>Zip file2: astrocytes ROS measured using DHE (Dihydroethidium)</p> <p>Zip file 3: astrocytes cell death measured using Sytox green</p>
BAF155 Methylation Drives Metastasis By Hijacking Super-enhancers and Subverting Anti-tumor Immunity
<p>Subunits of the chromatin remodeler SWI/SNF are the most frequently disrupted genes in cancer. However, how post-translational modifications (PTM) of SWI/SNF subunits elicit epigenetic dysfunction remains unknown. Arginine-methylation of BAF155 by coactivator-associated arginine methyltransferase 1 (CARM1) promotes triple negative breast cancer (TNBC) metastasis. Herein, we discovered the dual roles of methylated-BAF155 (me-BAF155) in promoting tumor metastasis: activation of super-enhanceraddicted oncogenes by recruiting BRD4, and repression of interferon / pathway genes to suppress host immune response. Pharmacological inhibition of CARM1 and BAF155 methylation not only abrogated the expression of an array of oncogenes, but also boosted host immune responses by enhancing the activity and tumor infiltration of cytotoxic T cells. Moreover, strong me-BAF155 staining was detected in circulating tumor cells from metastatic cancer patients. Despite low cytotoxicity, CARM1 inhibitors strongly inhibited TNBC cell migration in vitro, and growth and metastasis in vivo. These findings illustrate a unique mechanism of arginine methylation of a SWI/SNF subunit that drives epigenetic dysregulation, and establishes me-BAF155 as a therapeutic target to enhance immunotherapy efficacy.</p>
Population-level variation in parasite resistance due to differences in immune initiation and rate of response
<p>Closely related populations often differ in resistance to a given parasite, as measured by infection success or failure. Yet, the immunological mechanisms of these evolved differences are rarely specified. Does resistance evolve via changes to the host's ability to recognize that an infection exists, actuate an effective immune response, or attenuate that response? We tested whether each of these phases of the host response contributed to threespine sticklebacks' recently evolved resistance to their tapeworm <i>Schistocephalus solidus. </i>While marine stickleback and some susceptible lake fish permit fast-growing tapeworms, other lake populations are resistant and suppress tapeworm growth via a fibrosis response. We subjected lab-raised fish from three populations (susceptible marine 'ancestors', a susceptible lake population, a resistant lake population), to a novel immune challenge using an injection of: 1) a saline control, 2) alum, a generalized pro-inflammatory adjuvant that causes fibrosis, 3) a tapeworm protein extract, or 4) a combination of alum and tapeworm protein). With enough time, all three populations generated a robust fibrosis response to the alum treatments. Yet, only the resistant population exhibited a fibrosis response to the tapeworm protein alone. Thus, these populations differed in their ability to respond to the tapeworm protein but shared an intact fibrosis pathway. The resistant population also initiated fibrosis faster in response to alum, and was able to attenuate fibrosis, unlike the susceptible populations' slow but longer-lasting response to alum. As fibrosis has pathological side-effects that reduce fecundity, the faster recovery by the resistant population may reflect an adaptation to mitigate the costs of immunity. Broadly, our results confirm that parasite detection and immune initiation, activation speed, and immune attenuation simultaneously contribute to the evolution of parasite resistance and adaptations to infection in natural populations.</p>
Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection
<p><strong>scRNA-seq data</strong></p> <p>Data were processed using cellranger v 4.0.0 with the refdata-gex-GRCh38-2020-A reference.</p> <p><em>h5files.zip</em>: contains all h5-Files of raw feature-barcode counts (e.g. 20094_0001_A_B_raw_feature_bc_matrix.new.h5 )</p> <p><em>raw_feature_bc_matrices.zip</em>: contains the <em>same data</em> as h5files.zip, but also in mtx-format.</p> <p>covid_object_ncomms<em>.RDS</em>: contains the Seurat file with which all analyses were conducted.</p> <p><em>samples2condition.df</em>: text file containing sample to condition information</p> <p><strong>Bulk RNA-seq</strong></p> <p><em>covid_bulk.zip</em> contains the count matrices extracted from the zUMIs runs for the bulk cohort.</p> <p><em>nasal_swabs.zip</em> contains the count matrices extracted from the zUMIs run for the nasal swab cohort.</p> <p>The extracted count matrices were then used with the bulk analysis scripts provided with the source code.</p> <p><strong>Source Code</strong></p> <p>All <strong>source code</strong> for the publication is available from: <a href="https://github.com/mjoppich/covidSC">https://github.com/mjoppich/covidSC</a> or from tagged releases: <a href="https://github.com/mjoppich/covidSC/releases/tag/ncomms">https://github.com/mjoppich/covidSC/releases/tag/ncomms</a></p> <p>When using any of these data, please cite:<br> <br> Pekayvaz et al., Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection, Nature Communications 2022</p>
Self-adjuvanting Nanovaccines Boost Lung-resident CD4+ T Cell Immune Responses in BCG-primed mice
<p>The "readcount_genename.xls" file and "fpkm_genename.xls" file contain gene expression data for genes (gene list is detailed in "gene.xls") in the panel. All data were obtained from bone marrow derived dendritic cells from WT C57BL/6 mice treated with KFE8 nanofibers or mock. All RNA sequencing and subsequent processing was performed by Novogene Corporation.</p> <p>The remaining .xls files contain the differential expression analysis for KFE8 nanofiber treatment at four hours compared with mock (NF4vsC4) or KFE8 nanofiber treatment at sixteen hours compared with mock (NF16vsC16).</p> <p>The "pathway analysis Rcode.R" file contains the code used to generate Reactome pathway analysis for both time points. </p> <p>The "NF16 volc Rcode.R" file contains the code used to generate a volcano plot for the 16 hour time point. </p>
Single Cell Phenotypic Profiling to Identify a Set of Immune Cell Protein Biomarkers for Relapsed and Refractory Diffuse Large B Cell Lymphoma: A Single-Center Study
<p>Diffuse large B-cell lymphoma (DLBCL) is the most common invasive type of non-Hodgkin lymphoma. Cell-of-origin (COO) classification is related to patients’ prognoses. Primary drug resistance in treatment for DLBCL has been observed. The specific serum biomarkers in these patients who suffer from relapsed and refractory (R/R)-DLBCL remains unclear. In the current study, using single-cell RNA sequencing (scRNA-seq) and mass cytometry (CyTOF), we determined and verified immune cell biomarkers at the mRNA and protein levels in single-cell resolution from 18 diagnostic peripheral blood mononuclear cell (PBMC) specimens collected from patients with R/R DLBCL. As controls, five PBMC specimens from healthy volunteers were obtained. We identified a panel of 35 surface marker genes for the features of R/R DLBCL unique cell cluster by scRNA-seq of eight R/R DLBCL patient samples and validated its efficiency in an external cohort consisting of 10 R/R DLBCL patients by CyTOF. The cell clustering and dimension reduction were compared among R/R DLBCL samples in CyTOF Space with COO as well as the C-MYC expression designation. Immune cells from each patient occupied unique regions in the 32-dimensional phenotypic space with no apparent clustering of samples into discrete subtypes. Significant heterogeneity observed in subgroups was mainly attributed to individual differences among samples and not to expression differences in a single, homogeneous immune cell subpopulation. The marker panel showed reliability in labeling R/R DLBCL without any influence from COO stratification and C-MYC expression designation. Furthermore, we compared all the markers between R/R DLBCL and normal samples. A total of 12 biomarkers were significantly overexpressed in R/R DLBCL relative to the normal samples. Therefore, we further optimized the diagnostic biomarker panel of R/R DLBCL comprising CD82, CD55, CD36, CD63, CD59, IKZF1, CD69, CD163, CD14, CD226, CD84, and CD31. In summary, we developed a novel set of biomarkers for the diagnoses of patients with R/R DLBCL. Detections procedures at single-cell resolution provide precise biomarkers which may substantially overcome intertumoral and intratumoral heterogeneity among primary samples. The findings confirmed that each case was unique and may comprise multiple, genetically distinct subclones.</p> <p>Here we uploaded the dataset of CyTOF for external validation. For more detailed information, please contact Dr zheng (zenki_zheng@163.com)</p> <p> </p>
Immune disease risk variants regulate gene expression dynamics during CD4+ T cell activation
<p>During activation, T cells undergo extensive changes in gene expression which shape the properties of cells to exert their effector function. Therefore, understanding the genetic regulation of gene expression during T cell activation provides essential insights into how genetic variants influence the response to infections and immune diseases. We generated a single-cell map of expression quantitative trait loci (eQTL) across a T cell activation time-course. We profiled 655,349 CD4+ naive and memory T cells, capturing transcriptional states of unstimulated cells and three time points of cell activation in 119 healthy individuals. We identified 38 cell clusters, including stable clusters such as central and effector memory T cells and transient clusters that were only present at individual time points of activation, such as interferon-responding cells. We mapped eQTLs using a T cell activation trajectory and identified 6,407 eQTL genes, of which a third (2,265 genes) were dynamically regulated during T cell activation. We integrated this information with GWAS variants for immune-mediated diseases and observed 127 colocalizations, with significant enrichment in dynamic eQTLs. Immune disease loci colocalized with genes that are involved in the regulation of T cell activation, and genes with similar functions tended to be perturbed in the same direction by disease risk alleles. Our results emphasize the importance of mapping context-specific gene expression regulation, provide insights into the mechanisms of genetic susceptibility of immune diseases, and help prioritize new therapeutic targets.</p> <p>This dataset comprises of summary stats for eQTLs identified in the study (parquet files) and the ones which passed significance threshold (tensor_out.tar.gz archive). Files are described by cell subset (CD4 Naive, CD 4 Memory, TEMRA, TCM, etc.), time since activation (16h, 4h, 5days) as described in the publication (preprint https://doi.org/10.1101/2021.12.06.470953)</p>
Data and code for "Multi-omics Reveals Microbiome, Host Gene Expression, and Immune Landscape in Gastric Carcinogenesis" by Park et al., iScience 2022
<p>This repository is a part of the supplementary document in Park et al., "Multi-omics Reveals Microbiome, Host Gene Expression, and Immune Landscape in Gastric Carcinogenesis" published in iScience 2022.</p> <p>Abstract: To date, there has been no multi-omic analysis characterizing the intricate relationships between the intragastric microbiome and gastric mucosal gene expression in gastric carcinogenesis. Using multi-omic approaches, we provide a comprehensive view of the connections between the microbiome and host gene expression in distinct stages of gastric carcinogenesis (i.e., healthy, gastritis, cancer). We uncover associations specific to disease states. For example, uniquely in gastritis, Helicobacteraceae is highly correlated with the expression of <em>FAM3D</em>, which has been previously implicated in gastrointestinal inflammation. Additionally, in gastric cancer but not in adjacent gastritis, Lachnospiraceae is highly correlated with the expression of <em>UBD</em>, which regulates mitosis and cell cycle time. Furthermore, lower abundances of B cells in gastric cancer compared to gastritis may suggest a previously unidentified immune evasion process in gastric carcinogenesis. Our integrative analysis provides the most comprehensive description of microbial, host transcriptomic, and immune cell factors of the gastric carcinogenesis pathway.</p>
Adaptive immune response selects for increased body size - dataset
<p>The dataset for the manuscript " Adaptive immune response selects for increased body size ". The dataset is packed in ZIP archive 'Dataset_Ejsmond_etal_2022.zip' with variables and description of variables saved in Matlab workspaces.</p>
Raw data for the article: Successful Use of Heterologous CMV-Reactive T Lymphocyte to Treat Severe Refractory Cytomegalovirus (CMV) Infection in a Liver Transplanted Patient: Correlation of the Host Antiviral Immune Reconstitution with CMV Viral Load and CMV miRNome
<p>Cytomegalovirus (CMV) infection is the most significant viral infection in hosts with compromised immune systems as solid organ transplant patients. Despite significant progress being made in the prevention of CMV disease in these patients, further therapeutic strategies for CMV disease and for the CMV reactivation prevention are needed. Here, we describe the outcome of the infusion of in vitro expanded CMV-reactive T-cells, taken from a healthy CMV-seropositive donor, in a liver-transplanted recipient with a refractory recurrent CMV. In this particular case, adoptive transfer of allogenic CMV-reactive T-lymphocytes resulted in the clearance of CMV infection and resolution of the pathological manifestations of the patient. In the study we also investigated circulating miRNAs, both cellular and viral, as potential biomarkers during the course of CMV infection. The results indicate that the infusion of allogenic CMV-reactive T-cells can be an effective strategy to treat CMV infection recurrence when the generation of autologous virus specific T cell clones is not possible.</p>
Electromagnetic immune phosphor-tipped fibre-optic thermometers
<p>Calibration traceability can be broken where there are significant, unquantified uncertainties. Thermometry in harsh environments using electrical sensors, such as thermocouples or resistance thermometers, can be unpredictably affected by electro-magnetic sources. For this application, phosphor based temperature sensors with fibre-optic connection have been made following two different approaches – phosphor decay time changes and phosphor emission spectral changes – and tested by bombardment with high energy electrons and by measurements in large magnetic fields. Both sets of tests showed good immunity to exposure, and with magnetic field tests significantly better than a thermocouple. Phosphor thermometry therefore has potential to retain traceability in situations where conventional sensors might fail.</p>
Raw Data for the article: Klebsiella pneumoniae Lipopolysaccharides Serotype O2afg Induce Poor Inflammatory Immune Responses Ex Vivo
<p>Currently, <em>Klebsiella pneumoniae</em> is a pathogen of clinical relevance due to its plastic ability of acquiring resistance genes to multiple antibiotics. During <em>K. pneumoniae</em> infections, lipopolysaccharides (LPS) play an ambiguous role as they both activate immune responses but can also play a role in immune evasion. The LPS O2a and LPS O2afg serotypes are prevalent in most multidrug resistant <em>K. pneumoniae</em> strains. Thus, we sought to understand if those two particular LPS serotypes were involved in a mechanism of immune evasion. We have extracted LPS (serotypes O1, O2a and O2afg) from <em>K. pneumoniae</em> strains and, using human monocytes ex vivo, we assessed the ability of those LPS antigens to induce the production of pro-inflammatory cytokines and chemokines. We observed that, when human monocytes are incubated with LPS serotypes O1, O2a or O2afg strains, O2afg and, to a lesser extent, O2a but not O1 failed to elicit the production of pro-inflammatory cytokines and chemokines, which suggests a role in immune evasion. Our preliminary data also shows that nuclear translocation of NF-κB, a process which regulates an immune response against infections, occurs in monocytes incubated with LPS O1 and, to a smaller extent, with LPS O2a, but not with the LPS serotype O2afg. Our results indicate that multidrug resistant <em>K. pneumoniae</em> expressing LPS O2afg serotypes avoid an initial inflammatory immune response and, consequently, are able to systematically spread inside the host unharmed, which results in the several pathologies associated with this bacterium.</p>
Raw Data for the article: Impaired anti-SARS-CoV-2 humoral and cellular immune response induced by Pfizer-BioNTech BNT162b2 mRNA vaccine in solid organ transplanted patients
<p>SARS‐CoV‐2 vaccine is considered the primary health strategy able to end the current COVID‐19 pandemic. This viral infection impacts more severely solid organ transplant recipients (SOTRs) than general population, but the effect of vaccination in this subgroup of immunosuppressed patients is not known due to their exclusion from vaccination trials. Preliminary reports suggest a lower antibody production after BNT162b2 Pfizer/BioNTech mRNA‐vaccine,<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222937/#ajt16702-bib-0001"> 1 </a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222937/#ajt16702-bib-0002">2 </a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222937/#ajt16702-bib-0003">3 </a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222937/#ajt16702-bib-0004">4 </a>but no data are currently available on the elicited virus‐specific T cell responses.</p>
Parasite resistance and parasite tolerance: insights into transgenerational immune priming in an invertebrate host
<p>Parasites impose different selection regimes on their hosts, which respond by increasing their resistance and/or tolerance. Parental challenge with parasites can enhance the immune response of their offspring, a phenomenon documented in invertebrates and termed transgenerational immune priming. We exposed two parental generations of the model organism <em>Daphnia magna</em> to the horizontally-transmitted parasitic yeast <em>Metschnikowia bicuspidata</em>, and recorded resistance- and tolerance-related traits in the offspring generation. We hypothesized that parentally-primed offspring will increase either their resistance or their tolerance to the parasite. Our susceptibility assays revealed no impact of parental exposure on offspring resistance. Nonetheless, different fitness-related traits, which are indicative of tolerance, were altered. Specifically, maternal priming increased offspring production and decreased survival. Grandmaternal priming positively affected age at first reproduction and negatively affected brood size at first reproduction. Interestingly, both maternal and grandmaternal priming significantly reduced within-host parasite proliferation. Nevertheless, <em>Daphnia </em>primed for two consecutive generations had no competitive advantage in comparison to unprimed ones, implying additive maternal and grandmaternal effects. Our findings do not support evidence of transgenerational immune priming from bacterial infections in the same host species, thus emphasizing that transgenerational immune responses may not be consistent even within the same host species.</p>
Genetic covariance in immune measures and pathogen resistance in decorated crickets (Gryllodes sigillatus) is sex and pathogen specific
<p>Insects are important models for studying immunity in an ecological and evolutionary context. Yet, most empirical work on the insect immune system has come from phenotypic studies meaning we have a limited understanding of the genetic architecture of immune function in the sexes.</p> <p>We use nine highly inbred lines to thoroughly examine the genetic relationships between a suite of commonly used immune assays (haemocyte count, implant encapsulation, total phenoloxidase activity, antibacterial zone of inhibition, pathogen clearance) and resistance to infection by three generalist insect pathogens (the gram-negative bacterium <em>Serratia marcescens</em>, the gram-positive bacterium <em>Bacillus cereus</em> and the fungus <em>Metarhizium robertsii</em>) in male and female <em>Gryllodes sigillatus</em>.</p> <p>There were consistent positive genetic correlations between haemocyte count, antibacterial and phenoloxidase activity and resistance to <em>S. marcescens</em> in both sexes, but these relationships were less consistent for resistance to <em>B. cereus</em> and <em>M. robertsii</em>. In addition, the clearance of <em>S. marcescens</em> was genetically correlated with the resistance to all three pathogens in both sexes. Genetic correlations between resistances to the different pathogen species were inconsistent, indicating that resistance to one pathogen does not necessarily mean resistance to another. Finally, while there is ample genetic (co)variance in immune assays and pathogen resistance, these genetic estimates differed across the sexes and many of these measures were not genetically correlated across the sexes suggesting that these measures could evolve independently in the sexes.</p> <p>Our finding that the genetic architecture of immune function is sex and pathogen specific suggests that the evolution of immune function in male and female <em>G. sigillatus</em> is likely to be complex. Similar quantitative genetic studies that measure a large number of assays and resistance to multiple pathogens in both sexes are needed to ascertain if this complexity extends to other species.</p>
Data from: Condition-dependent immune function in a freshwater snail revealed by stable isotopes
<p>Data are saved as a tab-delimited text file (data.txt). Each row represents one snail individual.</p> <p> </p> <p>The file has the following columns:</p> <p>infection - trematode infection (0 = no, 1 = yes)</p> <p>PO_activity - PO-like activity of haemolymph</p> <p>antibacterial_activity - antibacterial activity of haemolymph</p> <p>shell_length - shell length (mm)</p> <p>faeces - amount of produced faeces (mg)</p> <p>d15N_faeces - δ<sup>15</sup>N value of faeces</p> <p>d13C_faeces - δ<sup>13</sup>C value of faeces</p> <p>C:N_faeces - C:N ration of faeces</p> <p>d15N_tissue - δ<sup>15</sup>N value of tissue</p> <p>d13C_tissue - δ<sup>13</sup>C value of tissue</p> <p>C:N_tissue - C:N ration of tissue</p>
Neutralizing immunity induced against the Omicron BA.2 variant in vaccinated and unvaccinated individuals infected by Omicron BA.1
<p>This repository contains the pertinent data files used in the manuscript, <em>Neutralizing immunity induced against the Omicron BA.2 variant in vaccinated and unvaccinated individuals infected by Omicron BA.1</em>.</p>
Dataset for the manuscript: Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages.
<p>Dataset for the manuscript:</p> <p>Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages. preprint, bioRxiv, 2022. DOI: 10.1101/2022.05.06.490883</p> <p>Each zip file contains the raw computational data (as a gzip compressed tarball), YAML input files, as well as Python plotting scripts. The Python plotting scripts have dependencies on the packages: <em>tarfile</em>, <em>multiprocessing</em>, <em>numpy</em>, <em>scipy</em>, and <em>matplotlib</em>. Note that the Python plotting scripts plot directly from the gzip compressed tarballs.</p> <p>The corresponding code can be found on GitHub: https://github.com/Ruth-Bowness-Group/CAModel</p>
A B cell actomyosin arc network couples integrin co-stimulation to mechanical force-dependent immune synapse formation
<p>B-cell activation and immune synapse (IS) formation with membrane-bound antigens are actin-dependent processes that scale positively with the strength of antigen-induced signals. Importantly, ligating the B-cell integrin, LFA-1, with ICAM-1 promotes IS formation when antigen is limiting. Whether the actin cytoskeleton plays a specific role in integrin-dependent IS formation is unknown. Here we show using super-resolution imaging of mouse primary B cells that LFA-1: ICAM-1 interactions promote the formation of an actomyosin network that dominates the B-cell IS. This network is created by the formin mDia1, organized into concentric, contractile arcs by myosin 2A, and flows inward at the same rate as B-cell receptor (BCR): antigen clusters. Consistently, individual BCR microclusters are swept inward by individual actomyosin arcs. Under conditions where integrin is required for synapse formation, inhibiting myosin impairs synapse formation, as evidenced by reduced antigen centralization, diminished BCR signaling, and defective signaling protein distribution at the synapse. Together, these results argue that a contractile actomyosin arc network plays a key role in the mechanism by which LFA-1 co-stimulation promotes B-cell activation and IS formation.</p>
A Monomeric Mycobacteriophage Immunity Repressor Utilizes Two Domains to Recognize an Asymmetric DNA Sequence
<p>Supporting source data consisting of simulation topologies and trajectories in pdb and xtc file formats, respectively.</p>
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Annotated Behaviour and Observability Dataset (ABODe)
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