Defective fetal liver erythropoiesis and T lymphopoiesis in mice lacking the phosphatidylserine receptor

Yuya Kunisaki, Sadahiko Masuko, Mayuko Noda, Ayumi Inayoshi, Terukazu Sanui, Mine Harada, Takehiko Sasazuki, Yoshinori Fukui

研究成果: Contribution to journalArticle査読

92 被引用数 (Scopus)

抄録

Clearance of apoptotic cells by macrophages is considered important for prevention of inflammatory responses leading to tissue damage. The phosphatidylserine receptor (PSR), which specifically binds to phosphatidylserine (PS) exposed on the surface of apoptotic cells, mediates uptake of apoptotic cells in vitro, yet the physiologic relevance of PSR remains unknown. This issue was addressed by generating PSR-deficient (PSR -/-) mice. PSR-/- mice exhibited severe anemia and died during the perinatal period. In the PSR-/- fetal livers, erythroid differentiation was blocked at an early erythroblast stage. In addition, PSR-/- embryos exhibited thymus atrophy owing to a developmental defect of T-lymphoid cells. Clearance of apoptotic cells by macrophages was impaired in both liver and thymus of PSR-/- embryos. However, this did not induce up-regulation of inflammatory cytokines. These results indicate that during embryonic development, PSR-mediated apoptotic cell uptake is required for definitive erythropoiesis and T lymphopoiesis, independently of the prevention of inflammatory responses.

本文言語英語
ページ(範囲)3362-3364
ページ数3
ジャーナルBlood
103
9
DOI
出版ステータス出版済み - 5 1 2004

All Science Journal Classification (ASJC) codes

  • 生化学
  • 免疫学
  • 血液学
  • 細胞生物学

フィンガープリント

「Defective fetal liver erythropoiesis and T lymphopoiesis in mice lacking the phosphatidylserine receptor」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル