期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2017
卷号：114
期号：47
页码：E10151-E10160
DOI：10.1073/pnas.1711345114
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：In secondary lymphoid organs, development and homeostasis of stromal cells such as podoplanin (Pdpn)–positive fibroblastic reticular cells (FRCs) are regulated by hematopoietic cells, but the cellular and molecular mechanisms of such regulation have remained unclear. Here we show that ablation of either signal regulatory protein α (SIRPα), an Ig superfamily protein, or its ligand CD47 in conventional dendritic cells (cDCs) markedly reduced the number of CD4+ cDCs as well as that of Pdpn+ FRCs and T cells in the adult mouse spleen. Such ablation also impaired the survival of FRCs as well as the production by CD4+ cDCs of tumor necrosis factor receptor (TNFR) ligands, including TNF-α, which was shown to promote the proliferation and survival of Pdpn+ FRCs. CD4+ cDCs thus regulate the steady-state homeostasis of FRCs in the adult spleen via the production of TNFR ligands, with the CD47–SIRPα interaction in cDCs likely being indispensable for such regulation.
关键词：dendritic cell ; fibroblastic reticular cell ; signal regulatory protein α ; CD47 ; tumor necrosis factor-α
