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These results suggest that IRF4 regulates the clonal expansion of CD8(+) T cells at least in part via the AKT signaling pathway. Moreover, IRF4 regulates the homeostatic proliferation of naive CD8(+) T cells, whereas the maintenance of memory CD8(+) T cells is IRF4-independent.
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IRF4 pathway is required for functional development of type 1 regulatory T cells.
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Data show that interferon regulatory factor 1 (IRF1) occupancy correlates with decreased interferon regulatory factor 4 (IRF4) abundance, suggesting an IRF1-IRF4-binding competition at the interleukin 9 (Il9) locus.
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Furthermore, chromatin immunoprecipitation (ChIP) followed by luciferase assays revealed direct binding of Foxo1 to both the Il9 and Irf4 promoters and induces their transactivation.
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MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression
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study identifies IRF4 as central regulator of TH1 responses and cellular metabolism. We propose that this function of IRF4 is fundamental for the initiation and maintenance of all TH cell responses.
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Nur77 suppresses CD4(+) T cell proliferation and uncover a suppressive role for Irf4 in TH2 polarization; halving Irf4 gene-dosage leads to increases in GATA3(+) and IL-4(+) cells.
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Muramyl dipeptide reduces fat inflammation and liver insulin resistance via NOD2. NOD1-activating muropeptides exacerbate glucose intolerance. IRF4 dictates insulin-sensitizing effects of NOD2, but not NOD1, muropeptides.
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Young mice had higher levels of IRF4 in the ischemic brains, suggesting that aging has a significant influence on stroke outcomes in mice, which is probably mediated by age-specific inflammatory responses.
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IRF4 is highly induced in graft-infiltrating T cells and is required for heart transplant rejection.
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The findings indicate that IRF4 functions as a central node in a TCR-responsive transcriptional circuit that establishes and sustains T cell exhaustion during chronic viral infection.
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RHS6 is a critical regulatory element for allergic airway inflammation and for coordinate regulation of Th2 cytokine genes by recruiting GATA3, SATB1, and IRF4.
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this study shows that epicutaneous sensitization to house dust mite allergen requires interferon regulatory factor 4-dependent dermal dendritic cells
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Cell fate and metabolic state are linked by transcriptional regulators, such as IRF4 and FoxO1, with dual roles in lineage and metabolic choice. Instructing some cells to utilize nutrients for anabolism and differentiation while other cells catabolically self-digest and self-renew may enable growth and repair in metazoa.
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Here the authors show that concomitant loss of Tet2 and Tet3 in mice at early B cell stage blocked the pro- to pre-B cell transition in the bone marrow, decreased Irf4 expression and impaired the germline transcription and rearrangement of the Igkappa locus.
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IRF4 protects arteries against neointima formation by promoting the expression of KLF4 by directly binding to its promoter.
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Data show that Fos-Related Antigen-2 (Fra-2) is a key upstream regulator of forkhead box O1 (Foxo1) and interferon regulatory factor 4 (Irf4) expression and influences proliferation and differentiation of B cells at multiple stages.
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GM-CSF can mediate inflammation and pain by regulating IRF4-induced CCL17 production
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MTORC2 operated in parallel with the IL-4Ralpha-Stat6 pathway.
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IRF4 mRNA and protein expression was remarkably suppressed during the development of myeloid-derived suppressor cells in the tumor microenvironment. IRF4 expression in MDSCs can modulate their activity to inhibit T cell proliferation through IL-10 production and ROS generation, and myeloid-specific deletion of IRF4 leads to the increase of MDSC differentiation. IRF4 reduction induced by tumors can increase MDSC numbers.
