| First Author | Nakahashi-Oda C | Year | 2012 |
| Journal | J Exp Med | Volume | 209 |
| Issue | 8 | Pages | 1493-503 |
| PubMed ID | 22826299 | Mgi Jnum | J:189144 |
| Mgi Id | MGI:5444542 | Doi | 10.1084/jem.20120096 |
| Citation | Nakahashi-Oda C, et al. (2012) Apoptotic cells suppress mast cell inflammatory responses via the CD300a immunoreceptor. J Exp Med 209(8):1493-503 |
| abstractText | When a cell undergoes apoptosis, phosphatidylserine (PS) is exposed on the outer leaflet of the plasma membrane. PS acts as an "eat-me" signal to direct phagocytes expressing PS receptors to engulf the apoptotic cell. We recently reported that the immunoreceptor CD300a, which is expressed on myeloid cells, is a PS receptor. We show that CD300a does not facilitate macrophage phagocytosis of apoptotic cells. Instead, CD300a delivers an inhibitory signal in mast cells to suppress production of LPS-induced inflammatory cytokines and chemokines. After cecal ligation and puncture (CLP), when a large number of cells undergo apoptosis in the peritoneal cavity, CD300a-deficient peritoneal mast cells produced more chemoattractant and recruited more neutrophils than did wild-type (WT) mast cells. As a result, CD300a-deficient mice showed increased neutrophil recruitment and improved bacterial clearance in the peritoneal cavity, and survived longer than WT mice. Antibody blockade of CD300a-PS interactions improved bacterial clearance and extended survival of WT mice subjected to CLP. These results indicated that CD300a is a nonphagocytic PS receptor that regulates mast cell inflammatory responses to microbial infections. |
