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Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [RNA-seq]

ABSTRACT: Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [RNA-seq]

PROVIDER: PRJNA989140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25073531_1.fastq.gz	Fastqsanger.gz
	SRR25073531_2.fastq.gz	Fastqsanger.gz
	SRR25073532_1.fastq.gz	Fastqsanger.gz
	SRR25073532_2.fastq.gz	Fastqsanger.gz
	SRR25073533_1.fastq.gz	Fastqsanger.gz

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Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation

Project description:Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation

| PRJNA989136 | ENA

Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [Fluidgm]

Project description:Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [Fluidgm]

| PRJNA989139 | ENA

Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [Fluidgm]

Project description:Commensal immune tolerance requires cells that actively sense and suppress inflammation. To understand how commensal tolerance works, mice colonized with recombinant Candida albicans expressing model MHC II peptide 2W1S were used to track CD4 cells with surrogate commensal specificity by tetramer staining and enrichement. Interestingly, half of the commensal CD4 cell lack expression of established T helper lineage defining transcription markers after intranuclear staining and flow cytometry. To more comprehensively investigate commensal cells, FACS sorted commensal CD4 cells with commensal specificity were analysed individually using single cell RNA sequencing.

2023-10-22 | GSE236150 | GEO

Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation [RNA-seq]

Project description:Commensal immune tolerance requires cells that actively sense and suppress inflammation. Here we show this is in large part mediated by CD4 cells that express the transcriptional regulator KLF2. Suppression by KLF2+ CD4 cells requires cell-intrinsic TCR stimulation. To investigate how KLF2 CD4 cells perform this role, gene expression by purified KLF2+ compared with KLF2-negative CD4 cells were evaluated with TCR stimulation in vitro and control non-stimulated cells.

2023-10-22 | GSE236148 | GEO

Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation.

Project description:Intestinal colonization by antigenically foreign microbes necessitates expanded peripheral immune tolerance. Here we show commensal microbiota prime expansion of CD4 T cells unified by the Kruppel-like factor 2 (KLF2) transcriptional regulator and an essential role for KLF2+ CD4 cells in averting microbiota-driven intestinal inflammation. CD4 cells with commensal specificity in secondary lymphoid organs and intestinal tissues are enriched for KLF2 expression, and distinct from FOXP3+ regulatory T cells or other differentiation lineages. Mice with conditional KLF2 deficiency in T cells develop spontaneous rectal prolapse and intestinal inflammation, phenotypes overturned by eliminating microbiota or reconstituting with donor KLF2+ cells. Activated KLF2+ cells selectively produce IL-10, and eliminating IL-10 overrides their suppressive function in vitro and protection against intestinal inflammation in vivo. Together with reduced KLF2+ CD4 cell accumulation in Crohn's disease, a necessity for the KLF2+ subpopulation of T regulatory type 1 (Tr1) cells in sustaining commensal tolerance is demonstrated.

| S-EPMC10822050 | biostudies-literature

Kruppel-like factor 2+ CD4 T cells avert microbiota induced intestinal inflammation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-22 | GSE236151 | GEO

Transcription profiling of thymocytes from Kruppel-like transcription factor (KLF)13 knock-out mice

Project description:Kruppel-like transcription factor (KLF)13, previously shown to regulate RANTES expression in vitro, is a member of the Kruppel- like family of transcription factors that controls many growth and developmental processes. To ascertain the function of KLF13 in vivo, Klf13-deficient mice were generated by gene targeting. As expected, activated T lymphocytes from Klf13-/- mice show decreased RANTES expression. However, these mice also exhibit enlarged thymi and spleens. TUNEL, as well as spontaneous and activation-induced death assays, demonstrated that prolonged survival of Klf13-/- thymocytes was due to decreased apoptosis. Microarray analysis suggests that protection from apoptosis-inducing stimuli in Klf13-/- thymocytes is due in part to increased expression of BCL-XL, a potent antiapoptotic factor. This finding was confirmed in splenocytes and total thymocytes by real-time quantitative PCR and Western blot as well as in CD4+CD8? single-positive thymocytes by real-time quantitative PCR. Furthermore, EMSA and luciferase reporter assays demonstrated that KLF13 binds to multiple sites within the Bcl-XL promoter and results in decreased Bcl-XL promoter activity, making KLF13 a negative regulator of BCL-XL.

2007-05-11 | E-SMDB-4035 | biostudies-arrayexpress

Kruppel-like transcription factor 13 regulates T lymphocyte survival in vivo.

2007-07-17 | GSE8497 | GEO

Inflammation durably imprints memory CD4+ T cells

Project description:Inflammation durably imprints memory CD4+ T cells

| PRJNA974831 | ENA

Transcriptome analysis of IFNγ producing and non-producing CD4 T cells during chronic intestinal inflammation.

Project description:Purpose: The goal of this study is to compare transcriptome profiles of IFNγ producing (Thy1.1+) and IFNγ non-producing (Thy1.1-) CD4 T cells during chronic intestinal inflammation using RNA sequencing. Methods: Total mRNA was isolated from FACS sorted CD44+Thy1.1+ and CD44+Thy1.1-CD4 T cells and sequenced in duplicate using Illumina HiSeq 2500 (2x100 base pair, paired-end reads). The sequence reads were aligned using mouse GRCm38.75 reference genome. DESeq2 software was used for differential expression analysis. Results: Differential expression analysis with DESeq2 algorithm revealed that a total of 942 and 1091 genes were significantly increased in the IFNγ+ and IFNγ- effector CD4 T cells, respectively (adjusted p value <0.05). We also performed gene set enrichment analysis (GSEA) by pre-ranking RNA sequencing data according to an adjusted p-value and the sign of differential expression. GSEA regults suggested that IFNγ+ CD4 T cells had terminally differentiated phenotype, while IFNγ- CD4 T cells had transcriptional profile associated with self-renewal and stemness. Conclusions: Our study suggests that effector CD4 T cells exist in a spectrum of differentiation status during chronic intestinal inflammation, which impacts pathogenicity of CD4 T cells.

2018-05-12 | GSE114346 | GEO

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