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• W2065635612 startingPage "821" @default.
• W2065635612 abstract "Interleukin (IL)-4 is a central regulator of T helper 2 (Th2) immune responses, and also has a major impact on innate immune cells. This cytokine primes macrophages for immune responses to parasites and induces a distinct macrophage phenotype that may also promote tissue repair. IL-4 signaling in macrophages is primarily mediated by the transcription factor signal transducer and activator of transcription 6 (Stat6), which in turn regulates a number of secondary DNA binding proteins that may participate in shaping the resulting phenotype. The impact of secondary transcription factors on IL-4-treated macrophages, however, is largely unknown. 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 dysregulated in Irf4-deficient macrophages. The presented data suggests a non-redundant role for Irf4 in shaping the phenotype of alternatively primed macrophages." @default.
• W2065635612 created "2016-06-24" @default.
• W2065635612 creator A5053584251 @default.
• W2065635612 creator A5067298809 @default.
• W2065635612 creator A5071128299 @default.
• W2065635612 date "2010-09-01" @default.
• W2065635612 modified "2023-10-02" @default.
• W2065635612 title "Interleukin-4 induced interferon regulatory factor (Irf) 4 participates in the regulation of alternative macrophage priming" @default.
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• W2065635612 doi "https://doi.org/10.1016/j.imbio.2010.05.031" @default.
• W2065635612 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20580461" @default.
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