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2,703 results for “CD4”
Antigen-specific CD4+ T cells exhibit distinct transcriptional phenotypes in the lymph node and blood following vaccination in humans
<p><strong>Abstract: </strong><br>SARS-CoV-2 infection and mRNA vaccination induce robust CD4+ T cell responses that are critical for the development of protective immunity. Here, we evaluated spike-specific CD4+ T cells in the blood and draining lymph node (dLN) of human subjects following BNT162b2 mRNA vaccination using single-cell transcriptomics. We analyze multiple spike-specific CD4+ T cell clonotypes, including novel clonotypes we define here using Trex, a new deep learning-based reverse epitope mapping method integrating single-cell T cell receptor (TCR) sequencing and transcriptomics to predict antigen-specificity. Human dLN spike-specific T follicular helper cells (TFH) exhibited distinct phenotypes, including germinal center (GC)-TFH and IL-10+ TFH, that varied over time during the GC response. Paired TCR clonotype analysis revealed tissue-specific segregation of circulating and dLN clonotypes, despite numerous spike-specific clonotypes in each compartment. Analysis of a separate SARS-CoV-2 infection cohort revealed circulating spike-specific CD4+ T cell profiles distinct from those found following BNT162b2 vaccination. Our findings provide an atlas of human antigen-specific CD4+ T cell transcriptional phenotypes in the dLN and blood following vaccination or infection.</p> <p><strong>More Information:</strong></p> <ul> <li><strong>Preprint:</strong> <a href="https://www.researchsquare.com/article/rs-3304466/v1">Research Square.</a></li> <li><strong>Sample information</strong>: data_inventory.csv file.</li> <li><strong>Code</strong> code_github_repo.zip or at the <a href="https://github.com/ncborcherding/COVID_TCR">original github repo</a></li> <li><strong>Interactive Portal</strong>: <a href="https://cellpilot.emed.wustl.edu/">CellPilot</a></li> </ul>
Data set of the manuscript titled: Follicular Immune Landscaping Reveals a distinct profile of FOXP3hi CD4+ T cells in Treated compared to Untreated HIV
<p>Multiplex imaging data were collected using a scanning confocal system (STELARIS, Leica) and proccessed with the Imaris and Fiji imaging programs. csv files incuding the position identifiers and intensities for each fluorochrome used were generated and data were further analysed using the FlowJo10 program. Neighboring analysis was performed using the G function and mean of minimum distances of relevant cell type pairs. </p>
In vivo treatment with insulin-like growth factor 1 reduces CCR5 expression on vaccine-induced activated CD4+ T-cells
<p>Dataset of the publication "In vivo treatment with insulin-like growth factor 1 reduces CCR5 expression on vaccine-induced activated CD4+ T-cells" by Bissa et al. on the journal Vaccines. </p><p>Each folder contains the original files reporting the data used to generate the manuscript.</p><p>For flowcytometry based assays the Flow panel is included in the folders. </p><p>For ELISA based assays the schemes of the plates are included in the folders. </p><p>The excel table "Bissa et al._Vaccines_2023_Animal IDs and viral acquisition" reports the IDs and grouping of the animals together with their viral acquisition</p><p>The excel table "Bissa et al._Vaccines_2023_Master table" reports each data used to generate the figures and supplemental materials included in the publication </p>
Code for: MHC Heterozygosity Prunes the Numbers of Different T Cell Receptors Expressed in CD4 T Cells
<p>Contains source data file and code for publication "MHC Heterozygosity Prunes the Numbers of Different T Cell Receptors Expressed in CD4 T Cells".<br>Associated FASTQ files are deposited on the NIH SRA under accession: PRJNA1106276</p>
TCRb sequencing of CD4+ and CD8+ T cells from hematological patients (part 1)
<p>This dataset contains TCRb sequencing of 177 samples from patients with aplastic anemia, myelodysplastic syndrome, immune thrombocytopenia, immunodeficiency or graft-versus-host disease and healthy controls. Samples are separated CD4+ or CD8+ cells from peripheral blood or bone marrow. The data has been produced with immunoSEQ platform (Adaptive Biotechnologies). The details regarding sample processing, sequencing and metadata can be found from the publication <em>Somatic mutations associate with clonal expansion of CD8+ T cells</em> (Lundgren et al, Science Advances, in press).</p> <p>The dataset is divided in 2 parts containing 91 (part 1) and 86 (part 2) files. Data is in immunoSEQ format (v2).</p>
Sex and Age Impact CD4+ T Cell Susceptibility to HIV In Vitro Through Cell Activation Dynamics
<p>Cellular composition and the responsiveness of the immune system evolve upon aging and are influenced by biological sex. CD4+ T cells from women living with HIV exhibit a decreased viral replication ex vivo compared to men's. We, thus, hypothesized that these findings could be recapitulated in vitro and infected primary CD4+ T cells with HIV-based vectors pseudotyped with VSV-G or HIV envelopes. We used cells isolated from twenty donors to interrogate the effect of sex and age on permissiveness over a six-day activation kinetics. Our data identified an increased permissiveness to HIV between 24 and 72 h post-stimulation. Sex- and age-based analyses at these time points showed an increased susceptibility to HIV of the cells isolated from males and from donors over 50 years of age, respectively. A parallel assessment of surface markers' expression revealed higher frequencies of activation marker CD69 and of immune checkpoint inhibitors (PD-1 and CTLA-4) in the cells from highly permissive donors. Furthermore, positive correlations were identified between the expression kinetics of CD69, PD-1 and CTLA-4 and HIV expression kinetics. The cell population heterogeneity was assessed using a single-cell RNA-Seq analysis and no cell subtype enrichment was identified according to sex. Finally, transcriptomic analyses further highlighted the role of activation in those differences with enriched activation and cell cycle gene sets in male and older female cells. Altogether, this study brought further evidence about the individual features affecting HIV replication at the cellular level and should be considered in latency reactivation studies for an HIV cure.</p>
Data for: The CD4 transmembrane GGXXG and juxtamembrane (C/F)CV+C motifs mediate pMHCII-specific signaling independently of CD4-Lck interactions
<p>We previously reported that the transmembrane GGXXG motif co-arose with the cytoplasmic juxtamembrane (C/F)CV+C motif in eutherian (placental mammal) CD4 and that constituent residues therein evolve under purifying selection (Lee, et al., 2022). These data led us to discover that mutating these motifs together increased CD4-Lck association but reduced CD3z, Zap70, and Plcg1 phosphorylation levels as well as IL-2 production. Because these mutants preferentially localized CD4-Lck pairs to non-membrane raft fractions, one potential explanation for our results was that they impaired proximal signaling by sequestering Lck away from TCR-CD3. An alternative hypothesis is that the mutations directly impacted TCR-CD3 signaling because the wild type motifs play a Lck-independent role in signaling. Here we used a reductionist approach to discriminate between these possibilities (Lee, et al., 2023). Our current data lead us to conclude that: intracellular CD4-Lck interactions are not necessary for pMHCII-specific signal initiation; the GGXXG and (C/F)CV+C motifs are key determinants of CD4-mediated pMHCII-specific signal amplification; the GGXXG and (C/F)CV+C motifs exert their functions independently of direct CD4-Lck association. These data provide a mechanistic explanation for why residues within these motifs are under purifying selection. The results are also important to consider for biomimetic engineering of synthetic receptors.</p>
Transcription start site analysis for heterogenous CD4+ T cells using 5′ scRNA-seq
<p>These datasets are generated by ReapTEC (read-level pre-filtering and transcribed enhancer call) using 5' single-cell RNA-seq data on human heterogenous CD4+ T cells. By taking advantage of a unique "cap signature" derived from the 5′-end of a transcript, ReapTEC simultaneously profiles gene expression and enhancer activity at nucleotide resolution using 5′-end single-cell RNA-sequencing (5′ scRNA-seq). The detail of ReapTEC pipeline is described in https://github.com/MurakawaLab/ReapTEC.</p>
Immune disease variants modulate gene expression in regulatory CD4+ T cells
<p>We mapped genetic regulation (QTL) of gene expression and chromatin activity in Tregs and we identified 133 colocalizing loci with immune disease variants.<br> For the time being, the preprint DOI: <a href="https://doi.org/10.1101/654632">10.1101/654632</a></p>
BCL6 deletion in CD4 T cells reveals Th2 eff mediated immunity in the skin
<p>RNA-Seq datasets related to the study of Mouse Tfh cells.</p> <p>Recent studies propose that Group 2 T follicular helper (Tfh) cells have a higher degree of functional plasticity in addition to their well-defined roles in mediating IL-4-dependent switching of germinal centre B cells to the production of IgG1 and IgE antibodies. In particular Tfh cells have been proposed to be an essential stage in Th2 effector cell development that are able to contribute to innate Type 2 responses. We used CD4-cre targeted deletion of BCL6 to identify the contribution Tfh cells make to tissue Th2 effector responses in models of skin atopic disease and lung immunity to parasites. Ablation of Tfh cells did not impair the development or recruitment of Th2 effector subsets to the skin and did not alter the transcriptional expression profile or functional activities of the resulting tissue resident Th2 effector cells. However, the accumulation of Th2 effector cells in lung Th2 responses was partially affected by BCL6 deficiency. These data indicate that the development of Th2 effector cells does not require a BCL6 dependent step implying Tfh and Th2 effector populations follow separate developmental trajectories and Tfh cells do not contribute to Type 2 responses in the skin . This study reveals important findings that add to the growing literature around the plasticity and functional interconversion of T helper subsets. </p>
N6-Methyladenosine Directly Regulates CD40L Expression In CD4+ T Lymphocytes
<p><strong>Abstract</strong></p> <p>T cell activation is a highly regulated process, modulated via the expression of various immune regulatory proteins including cytokines, surface receptors and co-stimulatory proteins. N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) is an RNA modification that can directly regulate RNA expression levels and it is associated with various biological processes. However, the function of m<sup>6</sup>A in T cell activation remains incompletely understood. We identify m<sup>6</sup>A as a novel regulator of the expression of CD40 ligand (CD40L) in human CD4<sup>+</sup> lymphocytes. Manipulation of the m<sup>6</sup>A ‘eraser’ fat mass and obesity-associated protein (FTO) and m<sup>6</sup>A ‘writer’ protein methyltransferase-like 3 (METTL3) directly affects the expression of CD40L. The m<sup>6</sup>A ‘reader’ protein YT521-B homology domain family-2 (YTHDF2) is able to recognize and bind m<sup>6</sup>A specific sequences on the <em>CD40L</em> mRNA and promotes its degradation. This study demonstrates that CD40L expression in human primary CD4<sup>+</sup> T lymphocytes is regulated via m<sup>6</sup>A modifications, elucidating a new regulatory mechanism in CD4<sup>+</sup> T cell activation that could possibly be leveraged in the future to modulate T cell responses in patients with immune-related diseases.</p> <p> </p> <p><strong>Data deposited</strong></p> <ul> <li>meRIP sequencing: read counts of healthy control peripheral blood-derived CD4+ T lymphocytes (figure 1 in article).</li> <li>meRIP sequencing: per gene TMM normalized log2(CPM + 0.168) expression values of healthy control peripheral blood-derived CD4+ T lymphocytes (figure 1 in article). Also includes Log2FoldChange values or each gene.</li> </ul>
Data from: Clone tracking through repeated malaria reveals high-fidelity CD4+ memory responses
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Transcription start site analysis for heterogenous CD4+ T cells using 5′ scRNA-seq
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Transcriptome Profiling of CD4+ T cell subpopulations from Aire-Knockout Rats
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Data for: The CD4 transmembrane GGXXG and juxtamembrane (C/F)CV+C motifs mediate pMHCII-specific signaling independently of CD4-Lck interactions
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Human memory CD4+ T cells recognize <em>Mycobacterium tuberculosis</em>-infected macrophages amid broader pathogen-specific responses
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Co-exposure of uranyl acetate and sodium arsenite differentially alters gene expression in CD3/CD28 activated CD4+ T-cells.
Communities in the western region of the United States experience environmental exposure to metal mixtures from living in proximity to numerous unremediated abandoned uranium mines. Metals including arsenic and uranium co-occur in and around these sites at levels higher than the United States Environmental Protection Agency maximum contaminant levels. To address the potential effect of these metals on the activation of CD4+ T-cells, we used RNA sequencing methods to determine the effect of exposure to uranyl acetate, sodium arsenite or a mixture of uranyl acetate and sodium arsenite. Oxidative stress is a mechanism proposed for metal toxicity, but findings for uranium differ across cell models. No significant changes in oxidative stress genes were detected for uranyl acetate, in contrast to sodium arsenite. Sodium arsenite induced a dose dependent effect on activation associated gene expression, targeting immune response genes at the lower dose. While uranyl acetate alone did not significantly alter activation associated gene expression, the mixture demonstrated a combined effect relative to sodium arsenite alone. The results demonstrate the need to investigate uranium alone and in metalloid mixtures at environmentally relevant concentrations to better understand the toxicological impact of these mixtures on T-cell activation, function and immune dysregulation.
Preexisting memory CD4 T cells in naïve individuals confer robust immunity upon vaccination
<p>Data set accompanying the publication "Preexisting memory CD4 T cells in naïve individuals confer robust immunity upon vaccination".</p> <p>In this study, we utilize high-throughput sequencing to profile the memory CD4 TCRβ repertoire and track vaccine-specific and epitope-specific TCRβ clonotypes following the de novo administration of hepatitis B (HepB) vaccine in healthy HepB-naïve individuals.</p> <p>The data set is comprised out of the following parts:</p> <ul> <li>repTCRb: Folder containing CD4+ TCR repertoire data from volunteers. Some of these samples are also available in ImmuneAccess (https://clients.adaptivebiotech.com/pub/deneuter-2018-cmvserostatus).</li> <li>peptideTCRab: Folder containing peptide-specific or peptide-pool-specific TCR data</li> <li>df_all: Meta and FC data for samples and volunteers</li> <li>freqCD154: CD154-based group definitions</li> <li>groups.csv: Group definitions used for classes</li> </ul>
Data from: Multi-omics analyses on rheumatoid arthritis in CD4+ T cells
<p><strong>Objective</strong>: CD4+ T cells have been suggested as the most disease-relevant cell type in rheumatoid arthritis (RA) in which RA-risk non-coding variants exhibit allele-specific effects on regulation of RA-driving genes. This study aimed to understand RA-specific signatures in CD4+ T cells using multi-omics data, interpreting inter-omics relationships in shaping the RA transcriptomic landscape.</p> <p><span><span><span><b>Methods</b>: We profiled genome-wide variants, gene expression, and DNA methylation in CD4<sup>+</sup> T cells from 82 RA patients and 40 healthy controls using high-throughput technologies. We investigated differentially expressed genes (DEGs) and differentially methylated regions (DMRs) in RA and localized quantitative trait loci (QTLs) for expression and methylation. We then integrated these based on individual-level correlations to inspect DEG-regulating sources and investigated the potential regulatory roles of RA-risk variants by a partitioned-heritability enrichment analysis with RA genome-wide association summary statistics.</span></span></span></p> <p><span><span><span><b>Results</b>: A large number of RA-specific DEGs were identified (n=2,575), highlighting T-cell differentiation and activation pathways. RA-specific DMRs, preferentially located in T-cell regulatory regions, were correlated with the expression levels of 548 DEGs mostly in the same topologically associating domains. In addition, expressional variances in 771 and 83 DEGs were partially explained by expression QTLs for DEGs and methylation QTLs for DEG-correlated DMRs, respectively. A large number of RA variants were moderately to strongly correlated with meQTLs. DEG-correlated DMRs, enriched with meQTLs, had strongly enriched heritability of RA.</span></span></span></p> <p><span><span><span><b>Conclusion</b>: Our findings revealed that the methylomic changes, driven by RA heritability-explaining variants, shape the differential expression of a substantial fraction of DEGs in CD4<sup>+</sup> T cells in RA patients, reinforcing the importance of a multi-dimensional approach in disease-relevant tissues.</span></span></span></p>
Coloc summary results for "Dissection of multiple sclerosis genetics identifies B and CD4+ T cells as driver cell subsets"
<p>Text files containing coloc results between MS GWAS loci and CD4 T and B cell cis-eQTLs from DICE. These results accompany the paper "<strong>Dissection of multiple sclerosis genetics identifies B and CD4+ T cells as driver cell subsets"</strong></p>
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