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Publication : Bone Marrow Endothelial Cells Take Up Blood-Borne Immune Complexes via Fcγ Receptor IIb2 in an Erythropoietin-Dependent Manner.

First Author  Ito T Year  2020
Journal  J Immunol Volume  205
Issue  8 Pages  2008-2015
PubMed ID  32907997 Mgi Jnum  J:303583
Mgi Id  MGI:6502455 Doi  10.4049/jimmunol.1901101
Citation  Ito T, et al. (2020) Bone Marrow Endothelial Cells Take Up Blood-Borne Immune Complexes via Fcgamma Receptor IIb2 in an Erythropoietin-Dependent Manner. J Immunol 205(8):2008-2015
abstractText  Immune complexes (ICs) in blood are efficiently removed mainly by liver reticuloendothelial systems consisting of sinusoidal endothelial cells and Kupffer cells expressing FcgammaR. The bone marrow (BM) also has sinusoidal vasculatures, and sinusoidal BM endothelial cells (BMECs) bear unique function, including hematopoietic niches and traffic regulation of hematopoietic cells. In this study, we found that sinusoidal BMECs express FcgammaRIIb2, which is markedly increased in anemic conditions or by the administration of erythropoietin (Epo) in healthy mice. BMECs expressed Epo receptor (EpoR), and the Epo-induced increase in FcgammaRIIb2 expression was abolished in Epor(-/-) ::HG1-Epor transgenic mice, which lack EpoR in BMECs except for BM erythroblasts, suggesting the effect was directly mediated via EpoR on BMECs. Further, although BMECs hardly captured i.v.-injected soluble ICs in healthy mice, Epo administration induced a remarkable increase in the uptake of ICs in a FcgammaRIIb-dependent manner. Enhancement of the IC incorporation capacity by Epo was also observed in cultured BMECs in vitro, suggesting the direct effect of Epo on BMECs. Moreover, we found that i.v.-injected ICs in Epo-treated mice were more rapidly removed from the circulation than in PBS-treated mice. These results reveal a novel function of BMECs to efficiently remove circulating blood-borne ICs in an FcgammaRIIb2-mediated manner.
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