TCR a/b profiling of thymic iNKT cells in Prkd2/3 mice (bulk TCR-seq)
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PROVIDER: PRJNA1214253 | ENA |
REPOSITORIES: ENA
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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
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
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
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
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
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.
2018-05-17 | GSE110327 | GEO
Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets
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Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets
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Project description:Thymic iNKT cells in Prkd2/3 mice (scRNA/TCR-seq, scATAC-seq)
| PRJNA1215692 | ENA
Project description:Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals
| PRJNA1064406 | ENA