Prion protein signaling induces M2 macrophage polarization and protects from lethal influenza infection in mice.

摘要: The cellular prion protein, PrPC, is a glycosylphosphatidylinositol anchored-membrane glycoprotein expressed most abundantly in neuronal and to lesser extent non-neuronal cells. Its conformational conversion into the amyloidogenic isoform neurons key pathogenic event diseases, including Creutzfeldt-Jakob disease humans scrapie bovine spongiform encephalopathy animals. However, normal functions of PrPC remain largely unknown, particularly Here we show that stimulation with anti-PrP monoclonal antibodies (mAbs) protected mice from lethal infection influenza A viruses (IAVs), abundant accumulation anti-inflammatory M2 macrophages activated Src family kinases (SFKs) infected lungs. SFK inhibitor dasatinib inhibited macrophage IAV-infected lungs after treatment mAbs abolished mAb-induced protective activity against mice. We also induced polarization peritoneal through activation vitro vivo. These results indicate could activate induce an phenotype mAbs, thereby eliciting IAVs mAbs. highlight as novel therapeutic target for IAV infection.