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

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

PROVIDER: PRJNA817591 | ENA |

REPOSITORIES: ENA

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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

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

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

2022-11-29 | GSE198967 | GEO

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

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

| PRJNA817586 | ENA

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

Project description:Single-cell RNA transcriptomics of thymic iNKT cells from BALB/c and Cd80/Cd86 -/- (B7KO) mice

| PRJNA817590 | ENA

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

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

2022-11-29 | GSE198970 | 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 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

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

TCR signal strength controls thymic differentiation of iNKT cell subsets

2018-05-17 | GSE110327 | GEO

Gene expression signatures of iNKT-subpopulations sorted from thymus of BALB/c and C57BL/6 mice

Project description:iNKT cells can be classified based on functional criteria into iNKT1, iNKT2 and iNKT17 cells, respectively. Here, a protocol was applied allowing sorting of living cells from thumus of BALB/c and C57BL/6 mice. The obtained gene expression profiles confirmed already existing information regarding the iNKT subtypes and will therefore provide useful hints for further investigations.

2016-10-05 | GSE69120 | GEO

TCR signal strength controls thymic differentiation of iNKT cell subsets.

Project description:During development in the thymus, invariant natural killer T (iNKT) cells commit to one of three major functionally different subsets, iNKT1, iNKT2, and iNKT17. Here, we show that T cell antigen receptor (TCR) signal strength governs the development of iNKT cell subsets, with strong signaling promoting iNKT2 and iNKT17 development. Altering TCR diversity or signaling diminishes iNKT2 and iNKT17 cell subset development in a cell-intrinsic manner. Decreased TCR signaling affects the persistence of Egr2 expression and the upregulation of PLZF. By genome-wide comparison of chromatin accessibility, we identify a subset of iNKT2-specific regulatory elements containing NFAT and Egr binding motifs that is less accessible in iNKT2 cells that develop from reduced TCR signaling. These data suggest that variable TCR signaling modulates regulatory element activity at NFAT and Egr binding sites exerting a determinative influence on the dynamics of gene enhancer accessibility and the developmental fate of iNKT cells.

| S-EPMC6037704 | biostudies-literature

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