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Park, Sung Ho
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B7-H3 regulates osteoclast differentiation via type I interferon-dependent IDO induction

DC Field Value Language Oh, Younseo ko Park, Robin ko Kim, So Yeon ko Park, Sung-ho ko Jo, Sungsin ko Kim, Tae-Hwan ko Ji, Jong Dae ko 2021-11-25T08:08:31Z - 2021-11-18 ko 2021-10 ko
dc.identifier.citation CELL DEATH & DISEASE, v.12, no.11, pp.971 ko
dc.identifier.issn 2041-4889 ko
dc.identifier.uri -
dc.description.abstract While their function, as immune checkpoint molecules, is well known, B7-family proteins also function as regulatory molecules in bone remodeling. B7-H3 is a receptor ligand of the B7 family that functions primarily as a negative immune checkpoint. While the regulatory function of B7-H3 in osteoblast differentiation has been established, its role in osteoclast differentiation remains unclear. Here we show that B7-H3 is highly expressed in mature osteoclasts and that B7-H3 deficiency leads to the inhibition of osteoclastogenesis in human osteoclast precursors (OCPs). High-throughput transcriptomic analyses reveal that B7-H3 inhibition upregulates IFN signaling as well as IFN-inducible genes, including IDO. Pharmacological inhibition of type-I IFN and IDO knockdown leads to reversal of B7-H3-deficiency-mediated osteoclastogenesis suppression. Although synovial-fluid macrophages from rheumatoid-arthritis patients express B7-H3, inhibition of B7-H3 does not affect their osteoclastogenesis. Thus, our findings highlight B7-H3 as a physiologic positive regulator of osteoclast differentiation and implicate type-I IFN-IDO signaling as its downstream mechanism. ko
dc.language 영어 ko
dc.publisher SPRINGERNATURE ko
dc.title B7-H3 regulates osteoclast differentiation via type I interferon-dependent IDO induction ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-85117682472 ko
dc.identifier.wosid 000709405900001 ko
dc.type.rims ART ko
dc.identifier.doi 10.1038/s41419-021-04275-6 ko
dc.identifier.url ko
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