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STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [RNA-Seq]

ABSTRACT: STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [RNA-Seq]

PROVIDER: PRJNA986546 | ENA |

REPOSITORIES: ENA

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STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [STAT4 CUT&RUN]

Project description:NK cells represent a cellular component of the mammalian innate immune system, and mount rapid responses against viral infection, including the secretion of the potent anti-viral effector cytokine IFN-g. Following mouse cytomegalovirus (MCMV) infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-g production during MCMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-g by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-g secretion by NK cells during viral infection.

2023-09-13 | GSE242911 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

2023-09-13 | GSE242900 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [RNA-Seq]

2023-09-13 | GSE235608 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [IL18R1KO RNA-seq]

2023-09-28 | GSE244300 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [STAT4 CUT&RUN]

Project description:STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [STAT4 CUT&RUN]

| PRJNA1015269 | ENA

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

Project description:STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

| PRJNA1015250 | ENA

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection

Project description:STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection

| PRJNA1015273 | ENA

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [IL18R1KO RNA-seq]

Project description:STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [IL18R1KO RNA-seq]

| PRJNA1022145 | ENA

Regulating type 1 IFN effects in CD8 T cells during viral infections: changing STAT4 and STAT1 expression for function

Project description:Type 1 IFNs can conditionally activate all of the signal transducers and activators of transcription molecules (STATs), including STAT4. The best-characterized signaling pathways use STAT1, however, and type 1 IFN inhibition of cell proliferation is STAT1 dependent. We report that type 1 IFNs can basally stimulate STAT1- and STAT4- dependent effects in CD8 T cells, but that CD8 T cells responding to infections of mice with lymphocytic choriomenigitis virus have elevated STAT4 and lower STAT1 expression with significant consequences for modifying the effects of type 1 IFN exposure. The phenotype was associated with preferential type 1 IFN activation of STAT4 as compared to STAT1. Stimulation through the TCR induced elevated STAT4 expression, and STAT4 was required for peak expansion of antigen-specific CD8 T cells, low STAT1 levels, and resistance to type 1 IFN-mediated inhibition of proliferation. Thus, a mechanism is discovered for regulating the consequences of type 1 IFN exposure in CD8 T cells, with STAT4 acting as a key molecule in driving optimal antigen-specific responses and overcoming STAT1-dependent inhibition of proliferation. CD8 T cells were purified from uninfected WT, STAT1-deficient and STAT4-deficient mice or from D8 LCMV-infected WT mice and either control treated or treated with 1x104 U mouse IFNalpha for 90 minutes.

2012-09-07 | E-GEOD-40666 | biostudies-arrayexpress

Regulating type 1 IFN effects in CD8 T cells during viral infections: changing STAT4 and STAT1 expression for function

2012-09-07 | GSE40666 | GEO