CD169⁺ macrophages provide a niche promoting erythropoiesis under homeostasis and stress.
CD169⁺ macrophages provide a niche promoting erythropoiesis under homeostasis and stress.
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巨噬细胞在红细胞生成中的作用是在几十年前通过描述骨髓（BM）中的“成红细胞岛”而提出的，所述成红细胞岛由被发育中的成红细胞包围的中央巨噬细胞组成。然而，巨噬细胞在体内稳态或疾病下的红细胞生成中的作用仍不清楚。CD169+巨噬细胞的特异性耗竭显著减少了BM中的成红细胞，但在稳态下未导致明显贫血，这可能是由于RBC清除率的伴随改变。然而，CD169+巨噬细胞耗竭显著损害了溶血性贫血、急性失血和骨髓消融的红细胞生成恢复。此外，在JAK2V617F驱动的真性红细胞增多症（PV）鼠模型中，巨噬细胞耗竭使红细胞区室正常化，表明PV中的红细胞生成出乎意料地保持在BM和脾微环境中的巨噬细胞的控制下。这些数据表明，CD169+巨噬细胞促进红细胞晚期成熟，巨噬细胞隔室的调节代表了治疗红细胞生成障碍的新策略。
The role of macrophages in erythropoiesis was suggested several decades ago with the description of “erythroblastic islands” in the bone marrow (BM) composed of a central macrophage surrounded by developing erythroblasts. However, the in vivo role of macrophages in erythropoiesis under homeostasis or disease remains unclear. Specific depletion of CD169+ macrophages markedly reduced erythroblasts in the BM but did not result in overt anemia under homeostasis likely due to concomitant alterations in RBC clearance. However, CD169+ macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation. Furthermore, macrophage depletion normalized the erythroid compartment in a JAK2V617F-driven murine model of polycythemia vera (PV), suggesting that erythropoiesis in PV, unexpectedly, remains under the control of macrophages in the BM and splenic microenvironments. These data indicate that CD169+ macrophages promote late erythroid maturation and that modulation of the macrophage compartment represents a novel strategy to treat erythropoietic disorders.
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压力红细胞生成：新信号和新的应激祖细胞。
影响因子：
3.2
作者：
Paulson RF;Shi L;Wu DC
通讯作者：
Wu DC
影响因子：
82.9
作者：
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影响因子：
5.4
作者：
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通讯作者：
FEIZI, T
DOI：
10.1084/jem.20101709
发表时间：
2011-05-09
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Hashimoto D;Chow A;Greter M;Saenger Y;Kwan WH;Leboeuf M;Ginhoux F;Ochando JC;Kunisaki Y;van Rooijen N;Liu C;Teshima T;Heeger PS;Stanley ER;Frenette PS;Merad M
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影响因子：
20.3
作者：
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通讯作者：
Beaumont, Carole