| First Author | Wei ZM | Year | 2019 |
| Journal | Immunol Res | Volume | 67 |
| Issue | 1 | Pages | 77-83 |
| PubMed ID | 30552619 | Mgi Jnum | J:295613 |
| Mgi Id | MGI:6454119 | Doi | 10.1007/s12026-018-9039-y |
| Citation | Wei ZM, et al. (2019) FcRgamma deficiency improves survival in experimental sepsis by down-regulating TLR4 signaling pathway. Immunol Res 67(1):77-83 |
| abstractText | Fc receptor common gamma signaling chain (FcRgamma), a common subunit shared by Fc receptors (FcgammaRI, III, IV, FcalphaRI, and FcepsilonRI), is an important immune regulator both in innate and adaptive immunity. Previous studies have shown that FcRgamma was a potential target of inflammatory diseases, whereas the role of FcRgamma in sepsis has been poorly understood. In this study, we found that deficiency of FcRgamma resulted in increased survival in lipopolysaccharide (LPS)/D-galactosamine and E. coli-induced sepsis in mice. This protective effect was characterized by decreased TNF-alpha, IL-6, and IL-10. Further experiments in bone marrow-derived macrophages (BMDMs) in vitro also showed that FcRgamma deficiency resulted in decreased production of TNF-alpha, IL-6, and IL-10 upon LPS stimulation. The mechanism study showed that FcRgamma was physiologically associated with toll-like receptor 4 (TLR4), and tyrosine phosphorylation of FcRgamma mediated TLR4 signaling pathway, followed by increased ERK phosphorylation upon LPS stimulation. Our results suggest that FcRgamma might be a potential therapeutic target of sepsis. |
