Here we show that interferon regulatory factor 4 (Irf4) is strongly induced on RNA and protein level in bone marrow-derived macrophages upon priming with IL-4. Using microarray-based whole genome expression analysis, we also demonstrate that a subset of IL-4 regulated genes, including several MHC-II genes, Ciita, Cyp1b1, and Il1rn, are ...

2023年8月1日 · In eosinophilic nasal polyps, IL-4 induces STAT6 signaling to upregulate IRF4 expression in epithelial cells and macrophages. IL-4 promotes EMT of hNECs through the STAT6/IRF4 signaling pathway. IL-4-induced M2 macrophages enhanced EMT of hNECs.

M1 macrophages play key roles in inflammation as well as antibacterial responses. IL4 and IL13 induce M2 polarity in macrophages. M2 transcriptomes are determined by different transcription factors such as IRF4, STAT6, JMJD3, PPARγ, PPARδ, and C/EBPβ. M2 macrophages exert anti-inflammatory activities such as tissue repair.

2016年10月13日 · IL-4 has been a model gene for studying the molecular mechanisms regulating the expression of Th2 cell-specific genes. Earlier studies focusing on the Il4 gene promoter have identified five binding sites for the NFAT/AP-1 complex, namely, P0, P1, P2, PRE-I/P4, and P5, forming the backbone of the Il4 promoter (Fig. 3.1).

2018年7月20日 · In this study, we report that IL4 also induces CCL17 production by acting through IRF4 in human monocytes and murine macrophages. Furthermore, evidence is presented that IL4 up-regulates IRF4 expression at the epigenetic level by enhancing the expression and activity of jumonji domain–containing protein 3 (JMJD3) demethylase.

本研究旨在探讨白细胞介素4（IL-4）/信号转导和转录激活因子6（STAT6）/干扰素调节因子4（IRF4）信号通路在嗜酸性CRSwNP EMT中的作用。 方法我们采用实时定量聚合酶链反应、免疫组织化学、免疫荧光染色和蛋白质印迹法来评估鼻窦粘膜样本中STAT6、IRF4和EMT标志物的表达。 使用来自嗜酸性粒细胞性 CRSwNP 患者的原代人鼻上皮细胞 (hNEC) 确定 IL-4 诱导的 EMT 效果。 进行伤口划痕试验、细胞形态学、蛋白质印迹和免疫荧光细胞化学来评估 EMT 和 …

干扰素调节因子4 (interferon regulatory factor 4, IRF4)为一种进化上极为保守的调控分子，在多种免疫细胞分化的关键阶段均不同程度表达，就其对固有免疫细胞谱系分化的作用而言，IRF4是参与调控M2样巨噬细胞极化、单核细胞衍生DC和常规DC2（conventional DC 2, cDC2)分化的 ...

We demonstrate that IRF4 potently synergizes with NFATc2 to specifically enhance NFATc2-driven transcriptional activation of the IL-4 promoter. This function is dependent on the physical interaction of IRF4 with NFATc2.

IRF4 synergizes with NFATc2 and the IL-4–inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to elicit significant levels of endogenous IL-4 production. Furthermore, naïve T helper cells from mice lacking IRF4 are compromised severely for the production of IL-4 and other Th2 cytokines.

In eosinophilic nasal polyps, IL-4 induces STAT6 signaling to upregulate IRF4 expression in epithelial cells and macrophages. IL-4 promotes EMT of hNECs through the STAT6/IRF4 signaling pathway. IL-4-induced M2 macrophages enhanced EMT of hNECs. Inhibition of STAT6 can downregulate the expression of …