Journal
NATURE IMMUNOLOGY
Volume 14, Issue 6, Pages 554-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2586
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [22116005, 24390021, 23790119, 24117724]
- Promoting Individual Research to Nurture the Seeds of Future Innovation and Organizing Unique Innovative Network (PRESTO) of Japan Science and Technology Agency
- Uehara Foundation
- Mitsubishi Foundation
- Terumo Foundation
- Mochida Foundation
- Toray Science Foundation
- Grants-in-Aid for Scientific Research [25460087, 22116003, 22116006, 24390021, 21390036, 22116002, 23590077, 23790120, 25860059, 22116001, 24117724, 10J02074, 23790119, 23591665, 23590067, 23659044, 22116005, 24619007] Funding Source: KAKEN
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Microenvironment-based alterations in phenotypes of mast cells influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A(2), regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD(2) synthase (L-PGDS) to provide PGD2, which facilitates mast-cell maturation via PGD2 receptor DP1. Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3-null or DP1-null mast cells, or mast cells cultured with L-PGDS-ablated fibroblasts exhibited impaired maturation and anaphylaxis of mast cells. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation.
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