| Literature DB >> 23624557 |
Yoshitaka Taketomi1, Noriko Ueno, Takumi Kojima, Hiroyasu Sato, Remi Murase, Kei Yamamoto, Satoshi Tanaka, Mariko Sakanaka, Masanori Nakamura, Yasumasa Nishito, Momoko Kawana, Naotomo Kambe, Kazutaka Ikeda, Ryo Taguchi, Satoshi Nakamizo, Kenji Kabashima, Michael H Gelb, Makoto Arita, Takehiko Yokomizo, Motonao Nakamura, Kikuko Watanabe, Hiroyuki Hirai, Masataka Nakamura, Yoshimichi Okayama, Chisei Ra, Kosuke Aritake, Yoshihiro Urade, Kazushi Morimoto, Yukihiko Sugimoto, Takao Shimizu, Shuh Narumiya, Shuntaro Hara, Makoto Murakami.
Abstract
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 A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 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.Entities:
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Year: 2013 PMID： 23624557 PMCID： PMC4065307 DOI： 10.1038/ni.2586
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606