Of macrophages and red blood cells; a complex love story

被引：230

作者：

de Back, Djuna Z. ^{[1
]}

Kostova, Elena B. ^{[1
]}

van Kraaij, Marian ^{[1
]}

van den Berg, Timo K. ^{[1
]}

van Bruggen, Robin ^{[1
]}

机构：

[1] Univ Amsterdam, Acad Med Ctr, Sanquin Res, Dept Blood Cell Res,Landsteiner Lab, NL-1105 AZ Amsterdam, Netherlands

来源：

FRONTIERS IN PHYSIOLOGY | 2014年 / 5卷

关键词：

red blood cell; macrophages; spleen; erythropoiesis; phagocytosis; NATURALLY-OCCURRING ANTI-BAND-3; ERYTHROID PROGENITOR CELLS; ERYTHROBLASTIC ISLAND FORMATION; ADHESION MOLECULE ICAM-4; MOUSE FETAL LIVER; BONE-MARROW; DEFINITIVE ERYTHROPOIESIS; APOPTOTIC CELLS; PHOSPHATIDYLSERINE EXPOSURE; PLASMODIUM-FALCIPARUM;

D O I：

10.3389/fphys.2014.00009

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Macrophages tightly control the production and clearance of red blood cells (RBC). During steady state hematopoiesis, approximately 10(10) RBC are produced per hour within erythroblastic islands in humans. In these erythroblastic islands, resident bone marrow macrophages provide erythroblasts with interactions that are essential for erythroid development. New evidence suggests that not only under homeostasis but also under stress conditions, macrophages play an important role in promoting erythropoiesis. Once RBC have matured, these cells remain in circulation for about 120 days. At the end of their life span, RBC are cleared by macrophages residing in the spleen and the liver. Current theories about the removal of senescent RBC and the essential role of macrophages will be discussed as well as the role of macrophages in facilitating the removal of damaged cellular content from the RBC. In this review we will provide an overview on the role of macrophages in the regulation of RBC production, maintenance and clearance. In addition, we will discuss the interactions between these two cell types during transfer of immune complexes and pathogens from RBC to macrophages.

引用

页数：11

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[21] Reduction of cell cycle progression in human erythroid progenitor cells treated with tumour necrosis factor alpha occurs with reduced CDK6 and is partially reversed by CDK6 transduction [J].