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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE242914 | GEO | 2023/09/13

REPOSITORIES: GEO

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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

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 [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 [RNA-Seq]

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

| PRJNA986546 | 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

STAT4-associated natural killer cell tolerance following liver transplantation.

Project description:OBJECTIVE:Natural killer (NK) cells are important mediators of liver inflammation in chronic liver disease. The aim of this study was to investigate why liver transplants (LTs) are not rejected by NK cells in the absence of human leukocyte antigen (HLA) matching, and to identify a tolerogenic NK cell phenotype. DESIGN:Phenotypic and functional analyses on NK cells from 54 LT recipients were performed, and comparisons made with healthy controls. Further investigation was performed using gene expression analysis and donor:recipient HLA typing. RESULTS:NK cells from non-HCV LT recipients were hypofunctional, with reduced expression of NKp46 (p<0.05) and NKp30 (p<0.001), reduced cytotoxicity (p<0.001) and interferon (IFN)-? secretion (p<0.025). There was no segregation of this effect with HLA-C, and these functional changes were not observed in individuals with HCV. Microarray and RT-qPCR analysis demonstrated downregulation of STAT4 in NK cells from LT recipients (p<0.0001). Changes in the expression levels of the transcription factors Helios (p=0.06) and Hobit (p=0.07), which control NKp46 and IFN? expression, respectively, were also detected. Hypofunctionality of NK cells was associated with impaired STAT4 phosphorylation and downregulation of the STAT4 target microRNA-155. Conversely in HCV-LT NK cell tolerance was reversed, consistent with the more aggressive outcome of LT for HCV. CONCLUSIONS:LT is associated with transcriptional and functional changes in NK cells, resulting in reduced activation. NK cell tolerance occurs upstream of major histocompatibility complex (MHC) class I mediated education, and is associated with deficient STAT4 phosphorylation. STAT4 therefore represents a potential therapeutic target to induce NK cell tolerance in liver disease.

| S-EPMC5284485 | biostudies-literature

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