复旦研究生《细胞免疫》Chemerin Peptides Promote Phagocytosis in a ChemR23-.pdfVIP

Europe PMC Funders Group Author Manuscript J Immunol. Author manuscript; available in PMC 2014 November 20. Published in final edited form as: J Immunol . 2010 May 1; 184(9): 5315–5324. doi:10.4049/jimmunol.0903378. E u Chemerin Peptides Promote Phagocytosis in a ChemR23- and r o p e Syk-Dependent Manner P M C Jenna L. Cash, Annabel R. Christian, and David R. Greaves F u Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom n d e r s Abstract A u Chemerin peptides represent a recently identified component of the endogenous anti-inflammatory t h o network that act via the G protein-coupled receptor ChemR23. The role of the chemerin peptide/ r M ChemR23 pathway in phagocytosis, the clearance of apoptotic cells (efferocytosis), and the a n resolution of inflammation is unknown. In this article, we report that low picomolar concentrations u s of the chemerin peptide chemerin15 (C15) enhance macrophage (MΦ) phagocytosis of microbial c r i particles and apoptotic cells by up to 360% in vitro. These prophagocytic effects of C15 are p t s significantly impaired in ChemR23−/− MΦs and are associated with increased actin polymerization and localization of F-actin to the phagocytic cup. Importantly, pharmacological inhibition of Syk activity completely abrogates the prophagocytic activities of C15 and associated changes in actin polymerization and phagocytic cup formation, suggesting that C15 promotes phagocytosis by facilitating phagocytic cup development in a Syk-dependent manner. During peritoneal