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Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals

ABSTRACT: Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals

PROVIDER: PRJNA1064406 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27536354_1.fastq.gz	Fastqsanger.gz
	SRR27536354_2.fastq.gz	Fastqsanger.gz
	SRR27536355_1.fastq.gz	Fastqsanger.gz
	SRR27536355_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals

Project description:Development of T cells is controlled by the signal strength of the TCR. The scaffold protein Kinase D-interacting substrate of 220 kDa (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell-specific Kidins220 knock-out (T-KO) mice have strongly reduced invariant natural killer T (iNKT) cell numbers and modest decreases in conventional T cells. Enhanced apoptosis due to increased TCR signaling in T-KO iNKT thymocytes of developmental stage 2 and 3 shows that Kidins220 downregulates TCR signaling at these stages. scRNAseq indicated that the transcription factor Aiolos is downregulated in Kidins220-deficient iNKT cells. Analysis of an Aiolos KO demonstrated that Aiolos is a downstream effector of Kidins220 during iNKT cell development. In the periphery, T-KO iNKT cells show reduced TCR signaling upon stimulation with α-galactosylceramide, suggesting that Kidins220 promotes TCR signaling in peripheral iNKT cells. Thus, Kidins220 reduces or promotes signaling dependent on the iNKT cell developmental stage.

2024-03-11 | GSE253196 | GEO

Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.

Project description:Development of T cells is controlled by the signal strength of the TCR. The scaffold protein kinase D-interacting substrate of 220 kilodalton (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell-specific Kidins220 knockout (T-KO) mice have strongly reduced invariant natural killer T (iNKT) cell numbers and modest decreases in conventional T cells. Enhanced apoptosis due to increased TCR signaling in T-KO iNKT thymocytes of developmental stages 2 and 3 shows that Kidins220 down-regulates TCR signaling at these stages. scRNA-seq indicated that the transcription factor Aiolos is down-regulated in Kidins220-deficient iNKT cells. Analysis of an Aiolos KO demonstrated that Aiolos is a downstream effector of Kidins220 during iNKT cell development. In the periphery, T-KO iNKT cells show reduced TCR signaling upon stimulation with α-galactosylceramide, suggesting that Kidins220 promotes TCR signaling in peripheral iNKT cells. Thus, Kidins220 reduces or promotes signaling dependent on the iNKT cell developmental stage.

| S-EPMC10942104 | biostudies-literature

Thymic iNKT cells in Prkd2/3 mice (scRNA/TCR-seq, scATAC-seq)

Project description:We have conducted single cell-RNA, -TCR, -ATAC sequencing (10x Genomics) to investigate a difference of gene expression, TCR repertoir and chromatin accesibility of thymic iNKT cells from wild-type and CD4-Cre-mediated T cell-specific Prkd2/3 doubly deficirnt (Prkd2/3ΔCD4) mice. Results demonstrate that Prkd2/3 are required for iNKT cell development and formaion of proper iNKT cell subtypes.

2025-09-08 | GSE288015 | GEO

TCR a/b profiling of thymic iNKT cells in Prkd2/3 mice (bulk TCR-seq)

Project description:We have conducted TCR a/b profiling to compare the usage of TCR a/b chains of thymic iNKT cells from wild-type (WT) and CD4-Cre-mediated T cell-specific Prkd2/3 doubly deficirnt (Prkd2/3ΔCD4) mice. Results demonstrate that top one frequent TCRa chain is identical, whereas usage of TCRb chain is different between WT and Prkd2/3ΔCD4 iNKT cells.

2025-09-08 | GSE287699 | GEO

Single-cell TCR transcriptomics of thymic iNKT cells from BALB/c and Cd80/Cd86 -/- (B7KO) mice

Project description:Single-cell TCR-seq analysis of murine thymic iNKT cells from three independent BALB/c mice and three independent Cd80/Cd86 (B7)-deficient mice

2022-11-29 | GSE198966 | GEO

The Effect of PRMT5 deficiency on thymic iNKT cells

Project description:Protein arginine methylation is a post-translational modification catalyzed by protein arginine methyltransferase (PRMT). To elucidate the role of PRMT5 in T cells, we generated T-cell specific PRMT5-deficient mice (Prmt5 flox/d Cd4-Cre mice) and found a severe loss of thymic iNKT cells as well as a reduced number in peripheral CD4+ and CD8+ T cells. As iNKT cells were significantly decreased in the stage 1, 2 and 3 of developmental stages, RNA-seq was performed using stage 1 iNKT cells of control and PRMT5-deficient mice. This transcriptome analysis will provide mechanistic insight into how PRMT5 contributes to thymic iNKT cell development.

2018-08-06 | GSE118135 | GEO

Ikaros-binding genomic sequences in mouse thymic iNKT cells and total thymocytes (ChIP-seq)

Project description:We have conducted ChIP-seq analysis to investigate Ikaros-regulating genes in mouse thymic iNKT cells. Total thyomcytes were also analyzed as a control. Results demonstrate that Ikaros-binding genomic sequences are different between total thymocytes and thymic iNKT cells.

2025-09-08 | GSE288329 | GEO

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets

| PRJNA436981 | ENA

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets

| PRJNA433481 | ENA

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:Three major phenotypically and functionally distinct invariant Natural Killer T (iNKT) cell subsets (iNKT1, iNKT17 and iNKT2), each with propensity to traffic to different tissues and to secrete different cytokines upon activation, have been defined. These fate assignments can be conferred upon iNKT cells during development in the thymus, but the cues that direct these decisions remain unclear. Here, we show that T cell antigen receptor (TCR) signal strength governs the development of iNKT cell subsets in the thymus, with high signaling strength necessary for iNKT2 and iNKT17 development. Alteration of TCR diversity and/or signaling dramatically diminished iNKT2 and iNKT17 cell subset development in a cell intrinsic manner. Decreased TCR signaling affected the persistence of Egr2 expression and the upregulation of PLZF both in vivo and in vitro. Genome-wide chromatin accessibility analysis revealed subset-specific activity of regulatory elements associated with unique signatures of transcription factor binding sites. NFAT and Egr binding motifs were found preferentially enriched in chromatin regulatory regions specifically accessible in iNKT2 cells that were lost in iNKT2 cells that had developed with reduced TCR signaling. Altogether, these data suggest a model of iNKT cell subset development where variable TCR signaling induces changes in chromatin accessibility at NFAT and Egr binding sites which exerts a determinative influence on the dynamic of gene enhancer accessibility that affects the developmental fate of iNKT cells.

2018-05-18 | GSE111427 | GEO

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