
NATURE . COM {
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Title:
JunB is essential for IL-23-dependent pathogenicity of Th17 cells | Nature Communications
Description:
CD4+ T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (TH17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic TH17 subsets share a common RORγt-dependent TH17 transcriptional programme, transcriptional regulatory mechanisms specific to each of these subsets are mostly unknown. Here we show that the AP-1 transcription factor JunB is critical for TH17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of RORγt and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic TH17 cells, but not in TGF-β1-dependent non-pathogenic TH17 cells. Junb-deficient T cells fail to induce TH17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic TH17 cells. The selective requirement of JunB for IL-23-dependent TH17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases. T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.
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cells, junb, pubmed, fig, article, mice, conditions, google, scholar, expression, supplementary, cas, thβ, induction, data, transcription, central, ila, nature, pathogenicity, cell, differentiation, batf, junbdeficient, rorγt, pathogenic, genes, control, irf, analysis, ildependent, stat, thpolarizing, activated, cdcrejunbflfl, biolegend, dna, nonpathogenic, tgfβ, factor, induced, foxp, function, signalling, binding, rorc, required, production, deficiency, inhibitor,
Topics {✒️}
nature portfolio privacy policy npo biotechnology research thermo fisher scientific editing th17-derived ifn-γ-producing cells advertising immune-specific ap-1-irf complexes junb-deficient th17-fate-mapping reporter cancer research chromatin solutions generated t-cell-specific junb-deficient horseradish peroxidase-conjugated anti-mouse wnt/β-catenin signaling contributes il-17a single-producing cells ifn-γ single-producing cells ires-driven complementary dna tgf-β1-dependent rorγt induction47 0/ reprints phycoerythrin-labelled il-17-secreting cells open boxes transferring junb-deficient cd4+cd45rbhicd25− eyfp+cd4+ t-cell population tgf-beta-induced foxp3 inhibits il-6/il-1β/il-23-induced th17 transforming-growth factor-beta plate-bound anti-cd3 antibody single base-pair resolution generate t-cell-specific pathogenic interferon-gamma-producing vivo th17-fate-mapping data ap-1-irf composite elements ap-1-irf composite elements33 tgf-β1-dependent th17 cells tgf-β/il-6-induced th17 cells t-cell receptor signalling cell-specific stat3-deficient mice junb-dependent il-23r induction tgf-β1/il-6-induced th17 anti-cd3 antibody treatment myelin oligodendrocyte glycoprotein-specific performed th17-fate-mapping analysis remove excess adaptor-dimer central nervous system cell-dependent iga responses transferring cd4+cd45rbhicd25− cells soluble anti-cd28 antibody library preparation library quantification il-17a-expressing cd4+
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headline:JunB is essential for IL-23-dependent pathogenicity of Th17 cells
description:CD4+ T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (TH17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic TH17 subsets share a common RORγt-dependent TH17 transcriptional programme, transcriptional regulatory mechanisms specific to each of these subsets are mostly unknown. Here we show that the AP-1 transcription factor JunB is critical for TH17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of RORγt and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic TH17 cells, but not in TGF-β1-dependent non-pathogenic TH17 cells. Junb-deficient T cells fail to induce TH17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic TH17 cells. The selective requirement of JunB for IL-23-dependent TH17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases. T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.
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headline:JunB is essential for IL-23-dependent pathogenicity of Th17 cells
description:CD4+ T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (TH17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic TH17 subsets share a common RORγt-dependent TH17 transcriptional programme, transcriptional regulatory mechanisms specific to each of these subsets are mostly unknown. Here we show that the AP-1 transcription factor JunB is critical for TH17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of RORγt and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic TH17 cells, but not in TGF-β1-dependent non-pathogenic TH17 cells. Junb-deficient T cells fail to induce TH17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic TH17 cells. The selective requirement of JunB for IL-23-dependent TH17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases. T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.
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