RT Journal Article
A1 Kunisaki, Yuya
A1 Masuko, Sadahiko
A1 Noda, Mayuko
A1 Inayoshi, Ayumi
A1 Sanui, Terukazu
A1 Harada, Mine
A1 Sasazuki, Takehiko
A1 Fukui, Yoshinori
T1 Defective fetal liver erythropoiesis and T lymphopoiesis in mice lacking the phosphatidylserine receptor
JF Blood
JO Blood
YR 2004
DO 10.1182/blood-2003-09-3245
VO 103
IS 9
SP 3362
OP 3364
SN 0006-4971
AB 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. (Blood. 2004;103:3362-3364)
RD 11/15/2025
UL https://doi.org/10.1182/blood-2003-09-3245