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- W4313305801 abstract "Abstract Intravenous Immunoglobulin (IVIG) is an anti-inflammatory drug used to treat various autoimmune conditions. Using the K/BxN model for rheumatoid arthritis we’ve shown that the therapeutic activity of IVIG depends on STAT6 signaling. Here we show that the anti-inflammatory activity of IL-4Rα induced STAT6 signaling takes place directly in LysM+ myeloid cells. However, in naïve mice these cells express low levels of the IL-4Rα. Exploring this discrepancy we found that during KBxN-mediated inflammation, IL-4Rα is highly up-regulated selectively on myeloid effector cells. This regulation is seen during several types of inflammation, and subsequently the cells respond to IL-4 with increased STAT6 phosphorylation. This regulation can be transferred both in vitro and in vivo using serum from mice with ongoing inflammation. Furthermore, transfer experiments show that the responsible (proteinase K-sensitive) factor is released by bone marrow derived non-lymphoid cells found in several organs, including the lungs and in fat. In conclusion, during ongoing inflammation, anti-inflammatory STAT6 signaling is specifically targeted to myeloid effector cells. This is mediated by regulation of the STAT6 signaling pathway by a secreted acute-phase reactant. We propose that this regulation is part of a homeostatic mechanism trying to limit excessive inflammation and tissue damage. IVIG, thus, exploits an endogenous feedback loop that could be further targeted for therapeutic purposes." @default.
- W4313305801 created "2023-01-06" @default.
- W4313305801 creator A5006790660 @default.
- W4313305801 date "2015-05-01" @default.
- W4313305801 modified "2023-09-25" @default.
- W4313305801 title "Myeloid cells are primed for anti-inflammatory STAT6 signaling during inflammation (CCR4P.210)" @default.
- W4313305801 doi "https://doi.org/10.4049/jimmunol.194.supp.118.10" @default.
- W4313305801 hasPublicationYear "2015" @default.
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