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KLF13 regulate memory-like CD8 T cells

ABSTRACT: “Memory-like T cells” are a subset of thymic cells that acquire effector function through the maturation process rather than interaction with specific antigen. Disruption of genes encoding T cell signaling proteins or transcription factors have provided insights into the differentiation of such cells. We show here that in BALB/c but not C57BL/6 mice, a large portion of thymic CD4-CD8+ T cells exhibit a memory-like phenotype. In BALB/c mice, IL-4 secreted by invariant natural killer T (iNKT) cells is both essential and sufficient for the generation of memory-like T cells. In C57BL/6 mice, iNKT cells are less abundant, producing IL-4 that is insufficient to induce thymic memory-like CD8+ T cells. BALB/c mice deficient in the transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6 mice and extremely low levels of thymic memory-like CD8+ T cells. This work documents the dramatic impact of a small number of KLF13-dependent iNKT cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE25502 | GEO | 2010/11/23

SECONDARY ACCESSION(S): PRJNA134641

REPOSITORIES: GEO

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KLF13 regulate memory-like CD8 T cells

Project description:“Memory-like T cells” are a subset of thymic cells that acquire effector function through the maturation process rather than interaction with specific antigen. Disruption of genes encoding T cell signaling proteins or transcription factors have provided insights into the differentiation of such cells. We show here that in BALB/c but not C57BL/6 mice, a large portion of thymic CD4-CD8+ T cells exhibit a memory-like phenotype. In BALB/c mice, IL-4 secreted by invariant natural killer T (iNKT) cells is both essential and sufficient for the generation of memory-like T cells. In C57BL/6 mice, iNKT cells are less abundant, producing IL-4 that is insufficient to induce thymic memory-like CD8+ T cells. BALB/c mice deficient in the transcription factor Kruppel-like factor (KLF) 13 have comparable numbers of iNKT cells to C57BL/6 mice and extremely low levels of thymic memory-like CD8+ T cells. This work documents the dramatic impact of a small number of KLF13-dependent iNKT cells. FACS-sorted naive splenic CD8 T cells from wild type and KLF13 ko mice were compared.

2010-11-23 | E-GEOD-25502 | biostudies-arrayexpress

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

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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 C57BL/6 and Hivep3-/- mice

Project description:Single-cell RNA-seq analysis of murine thymic iNKT cells from two independent C57BL/6 mice and two independent Hivep3-deficient mice

2020-11-06 | GSE152786 | GEO

KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [RNA-seq]

Project description:Although significant progress has been achieved in elucidating the genetic architecture of systemic lupus erythematosus (SLE), identifying genes underlying the pathogenesis has been challenging. The NZM2410-derived lupus susceptibility Sle3 locus is associated with T cell hyperactivity and activated myeloid cells. However, candidate genes associated with these phenotypes have not been identified. Here, we narrow the Sle3 locus to a smaller genomic segment (Sle3k) and show that mice carrying Sle3k and Sle1 loci developed lupus nephritis. We identify Klf13 as the primary candidate gene upregulated in Sle3k mice and demonstrate that Klf13 upregulation is associated with genome-wide transcription changes resulting in higher levels of proinflammatory cytokines, enhanced T cell activation, and hyperresponsiveness of myeloid cells. Correspondingly, Klf13 –/– mice display striking repression of genes involved in mediating immune activation, including key proinflammatory cytokines/chemokines. Furthermore, Klf13 –/– mice show profound dysregulation in cytokine signaling pathways in myeloid cells in response to toll receptor ligands, thus revealing a key role of KLF13 in modulating myeloid cell function. Klf13 upregulation is associated with increased production of RANTES, a key chemokine in lupus nephritis, in activated T cells and the kidneys of lupus-prone mice. In sum, our findings reveal Klf13 as a key gene in the Sle3 interval in mediating lupus pathogenesis that may have implications in the rational design of new therapies for SLE and other autoimmune/inflammatory diseases.

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KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [ATAC-seq]

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ATAC-seq analysis of murine thymic iNKT subsets from C57BL/6 mice and Hivep3-deficient mice

Project description:ATAC-seq analysis of murine thymic iNKT subsets from two independent C57BL/6 mice and two independent Hivep3-deficient mice

2020-10-31 | GSE160518 | 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

Mus musculus

Project description:KLF13 regulate memory-like CD8 T cells

| PRJNA134641 | ENA

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

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