Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 209, Issue 8, Pages 1493-1503Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20120096
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- National Institute of Biomedical Innovation (NIBIO), Japan
- Grants-in-Aid for Scientific Research [24390205, 22390073, 24659175, 24590550, 24659176, 23390091, 22000013, 23592664] Funding Source: KAKEN
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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.
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