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- W4313359588 abstract "Abstract IFN-γ promotes the expression of anti-viral and anti-tumoral genes which act intrinsically to the cell (e.g. ISG54, ISG49), as well as genes which express secreted factors (e.g. IP10, IL-15). The canonical pathway of the IFN-γ receptor (IFNGR) revolves around the phosphorylation of the transcription factor, STAT1, promoting its dimerization and localization to the nucleus where it induces the expression of target genes, like Interferon Regulatory Factor 1 (IRF1). Our lab has shown impaired IFNGR signaling in cells which do not express IRF3. IRF3 is a transcription factor canonically activated by Pathogen Associated Molecular Patterns (PAMPs) through Pattern Recognition Receptors (PRRs) like Toll-Like Receptor 3 (TLR3). TLR3 recognizes dsRNA and analogs like Polyinosinic-polycytidylic acid (Poly I:C). WT and IRF3KO RAW 264.7 cell lines expressing secreted luciferase (Lucia) under control of an ISG54 promoter were stimulated with IFN-γ, Poly I:C, or both. IRF3KO RAW-Lucia cells had significantly reduced ISG54 promoter activity in response to all treatments compared with WT RAW-Lucia. This was confirmed via western blot and qPCR analysis. Using qPCR, expression of ISG49 and IL-15 was also IRF3 dependent in response to all treatments. However, expression of IP10 was only IRF3 dependent in response to Poly I:C and not IFN-γ. Thioglycollate elicited peritoneal macrophages (PECs) generated from WT and IRF3KO mice also showed an IRF3 dependency for the expression of ISG54 in response to IFN-γ. These PECs did not show altered STAT1 phosphorylation or IRF1 expression. These data imply that IRF3 contributes to the non-canonical pathway of IFNGR signaling." @default.
- W4313359588 created "2023-01-06" @default.
- W4313359588 creator A5004179450 @default.
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- W4313359588 date "2018-05-01" @default.
- W4313359588 modified "2023-09-27" @default.
- W4313359588 title "A Non-Canonical Role for Interferon Regulatory Factor 3 Downstream of the Interferon Gamma Receptor" @default.
- W4313359588 doi "https://doi.org/10.4049/jimmunol.200.supp.109.21" @default.
- W4313359588 hasPublicationYear "2018" @default.
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