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IRF4 modulates CD8 T cell sensitivity to IL-2 family cytokines

ABSTRACT: The purpose of this study is to identify expression differences between wild type CD8 T cells vs IRF4 knock out CD8 T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE101510 | GEO | 2018/01/01

SECONDARY ACCESSION(S): PRJNA394704

REPOSITORIES: GEO

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IRF4 Modulates CD8+ T Cell Sensitivity to IL-2 Family Cytokines.

Project description:IFN regulatory factor 4 (IRF4) is a key transcription factor that promotes effector CD8+ T cell differentiation and expansion. The roles of IRF4 in regulating the CD8+ T cell response to cytokines have not been explored. In this article, we show that IL-2 and IL-15 signaling and STAT5 activation regulate IRF4 expression in CD8+ T cells. Gene-expression profile analysis has also revealed that IRF4 is required for expression of the receptors of IL-2 family cytokines CD122 and CD127. We found that IRF4 binds directly to CD122 and CD127 gene loci, indicating that it may directly promote CD122 and CD127 gene transcription. As a consequence, IRF4-deficient CD8+ T cells show diminished sensitivity to IL-2, IL-15, and IL-7 treatment in vitro. Furthermore, we found that IRF4-deficient CD8+ T cells had lower expression of CD122 and CD127 in vivo during influenza virus infection. These data suggest that IRF4 regulates the sensitivity of CD8+ T cells to IL-2 family cytokines, which correlates with the diminished effector and memory CD8+ T cell responses in IRF4-deficient CD8+ T cells.

| S-EPMC5858712 | biostudies-literature

The transcription factor IRF4 impedes human CD8 T-cell function and promotes cells proliferation and PD-1 expression

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The Transcription Factor IRF4 Determines the Anti-Tumor Immunity of CD8+ T cells

Project description:Four TIL populations from B16-F10 melanoma were analyzed by scRNA-seq, including adoptively transterred anti-tumor CD8+ Pmel-1 T cells that were transduced with IRF4 (sample 1, IRF4_Pmel) or GFP control (Sample 3, Ctrl_Pmel), and CD45+ endogenous TILs from either the IRF4 group (Sample 2, IRF4_TILs) or Ctrl group (Sample 4, Ctrl_TILS).

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ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

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Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells.

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Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation. Two-condition experiment, IRF4 -/- vs IRF4 +/- Th17 cells at 42hrs. Biological replicates: 3 for each condition

2012-09-13 | E-GEOD-40726 | biostudies-arrayexpress

IRF4 haploinsufficiency in a family with Whipple’s disease

Project description:IRF4 haploinsufficiency in a family with Whipple’s disease

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