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Murine cytotoxic CD4 T cells

ABSTRACT: Murine cytotoxic CD4 T cells

PROVIDER: PRJNA743066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15015700_1.fastq.gz	Fastqsanger.gz
	SRR15015700_2.fastq.gz	Fastqsanger.gz
	SRR15015701_1.fastq.gz	Fastqsanger.gz
	SRR15015701_2.fastq.gz	Fastqsanger.gz
	SRR15015702_1.fastq.gz	Fastqsanger.gz

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Murine cytotoxic CD4 T cells

Project description:Cytotoxic CD4 T lymphocytes (CD4-CTL) are important in anti-viral immunity.  For example, we have previously shown that in mice, CD4-CTL are important to control ectromelia virus (ECTV) infection.  How viral infections induce CD4-CTL responses remains incompletely understood. Here we demonstrate that not only ECTV but also vaccinia virus and Lymphocytic Choriomeningitis virus induce CD4-CTL, but that the response to ECTV is stronger.  Using ECTV, we also demonstrate that in contrast to CD8-CTL, CD4-CTL differentiation requires constant virus replication and ceases once the virus is controlled.  We also show that Major Histocompatibility Complex Class II molecules on CD11c+ cells are required for CD4-CTL differentiation and for mousepox resistance.  Transcriptional analysis indicated that anti-viral CD4-CTL and non-cytolytic T Helper 1 (Th1) CD4 T cells have similar transcriptional profiles, suggesting that CD4-CTL are terminally differentiated classical Th1 cells.  Interestingly, CD4-CTL and classical Th1 cells expressed similar mRNA levels of the transcription factors ThPOK and GATA-3, necessary for CD4 T cell linage commitment; and Runx3, required for CD8 T cell development and effector function.  However, at the protein level, CD4-CTL had higher levels of the three transcription factors suggesting that further post-transcriptional regulation is required for CD4-CTL differentiation.  Finally, using CRISPR-Cas9 deletion of Runx3 in CD4 T cells, we demonstrate that the development of CD4-CTL but not of classical Th1 CD4 T cells requires Runx3 following ECTV infection.  These results further our understanding of the mechanisms of CD4-CTL differentiation during viral infection and the role of post-transcriptionally regulated Runx3 in this process.

2021-07-06 | GSE179289 | GEO

Comparision of expression profile between CD4+ helper T cells and CD8+ cytotoxic T cells

Project description:We compared gene expression profiling between CD4+ helper T cells and CD8+ cytotoxic T cells CD4+ helper T cells vs CD8+ cytotoxic T cells

2015-06-30 | E-GEOD-67204 | biostudies-arrayexpress

Genome-wide study of methylation profile of human cytotoxic CD4 T cells

Project description:The methylation profile of human cytotoxic CD4 T cells was compared to their naive counterpart, to central memory Th1 cells, and to naive and cytotoxic CD8 T cells in order to elucidate the epigenetic basis of cytotoxic differentiation in CD4 T cells.

2018-03-06 | GSE75405 | GEO

Genome-wide study of transcriptional profile of human cytotoxic CD4 T cells

Project description:The transcriptional profile of human cytotoxic CD4 T cells was compared to their naive counterpart, to central memory Th1 cells, and to naive and cytotoxic CD8 T cells in order to elucidate the epigenetic basis of cytotoxic differentiation in CD4 T cells.

2018-03-06 | GSE75404 | GEO

Concomitant Cytotoxic Effector Differentiation of CD4+ and CD8+ T Cells in Response to EBV-Infected B Cells

Project description:Most people infected by EBV acquire specific immunity, which then controls latent infection throughout their life. Immune surveillance of EBV-infected cells by cytotoxic CD4+ T cells has been recognized; however, the molecular mechanism of generating cytotoxic effector T cells of the CD4+ subset remains poorly understood. Here we compared phenotypic features and the transcriptome of EBV-specific effector-memory CD4+ T cells and CD8+ T cells in mice and found that both T cell types show cytotoxicity and, to our surprise, widely similar gene expression patterns relating to cytotoxicity. Similar to cytotoxic CD8+ T cells, EBV-specific cytotoxic CD4+ T cells from human peripheral blood expressed T-bet, Granzyme B, and Perforin and upregulated the degranulation marker, CD107a, immediately after restimulation. Furthermore, T-bet expression in cytotoxic CD4+ T cells was highly correlated with Granzyme B and Perforin expression at the protein level. Thus, differentiation of EBV-specific cyto toxic CD4+ T cells is possibly controlled by mechanisms shared by cytotoxic CD8+ T cells. T-bet-mediated transcriptional regulation may explain the similarity of cytotoxic effector differentiation between CD4+ T cells and CD8+ T cells, implicating that this differentiation pathway may be directed by environmental input rather than T cell subset.

2022-08-26 | GSE206802 | GEO

Eomes is sufficient to regulate IL-10 expression and cytotoxic effector molecules in murine CD4+ T cells

Project description:Eomes is sufficient to regulate IL-10 expression and cytotoxic effector molecules in murine CD4+ T cells

| PRJNA883404 | ENA

Comparision of expression profile between CD4+ helper T cells and CD8+ cytotoxic T cells

Project description:We compared gene expression profiling between CD4+ helper T cells and CD8+ cytotoxic T cells

2015-06-30 | GSE67204 | GEO

Imbalance of regulatory and cytotoxic SARS-CoV-2-reactive CD4+ T cells in COVID-19

Project description:The contribution of CD4+ T cells to protective or pathogenic immune responses to SARS-CoV-2 infection remains unknown. Here, we present a large-scale single-cell transcriptomic analysis of viral antigen-reactive CD4+ T cells from 40 COVID-19 patients. In hospitalized patients compared to non-hospitalized patients, we found increased proportions of cytotoxic follicular helper (TFH) cells and cytotoxic T helper cells (CD4-CTLs) responding to SARS-CoV-2, and reduced proportion of SARS-CoV-2-reactive regulatory T cells (TREG). Importantly, in hospitalized COVID-19 patients, a strong cytotoxic TFH response was observed early in the illness which correlated negatively with antibody levels to SARS-CoV-2 spike protein. Polyfunctional T helper (TH)1 and TH17 cell subsets were underrepresented in the repertoire of SARS-CoV-2-reactive CD4+ T cells compared to influenza-reactive CD4+ T cells. Together, our analyses provide so far unprecedented insights into the gene expression patterns of SARS-CoV-2-reactive CD4+ T cells in distinct disease severities.

2020-10-06 | GSE152522 | GEO

Identification of human exTregs as CD16+CD56+ cytotoxic CD4+ T cells.

Project description:Identification of human exTregs as CD16+CD56+ cytotoxic CD4+ T cells.

| PRJNA896569 | ENA

Single cell sequencing reveals expanded cytotoxic CD4+ T cells and two clusters of peripheral helper T cells in synovial fluid of ACPA+ RA patients

Project description:Rheumatoid arthritis is an autoimmune disease affecting the synovial joints where CD4+ T cells play a pathogenic role. However, a deeper analysis of cytotoxic CD4+ T cells is still lacking, particularly in the context of the recently described peripheral helper T-cell subset (TPH). Here, we show, using 10X-single-cell sequencing and multi-parameter flow cytometry that cytotoxic CD4+ T cells are enriched in synovial fluid (SF) of anti-citrullinated peptides antibody (ACPA)-positive RA patients. We also identify two distinct TPH clusters differentially characterized by the expression of CXCL13 and PRDM1, respectively. Our data reveal that the adhesion G-Protein Coupled Receptor 56 (GPR56), a marker of circulating cytotoxic cells, delineates the TPH CD4+ T-cell subset in SF. At the site of inflammation, GPR56+ CD4+ T cells expressed the tissue-resident memory markers LAG-3, CXCR6, and CD69. Further, TCR clonality analysis revealed that most of the expanded clones in PB and SF are contained within the cytotoxic CD4+ T-cell population. Finally, the detection of common TCRs between the two TPH and cytotoxic CD4+ T cell clusters suggests a common differentiation pathway between these three subsets. Our study provides a better overview of the different pathogenic T-cell subsets at the site of inflammation in ACPA+ RA and suggests GPR56 as a therapeutic target to modulate TPH cells and cytotoxic CD4+ T cell function.

| EGAS00001005241 | EGA

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