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B7-H3 regulates osteoclast differentiation via type I interferon-dependent IDO induction

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Title
B7-H3 regulates osteoclast differentiation via type I interferon-dependent IDO induction
Author
Oh, YounseoPark, RobinKim, So YeonPark, Sung-hoJo, SungsinKim, Tae-HwanJi, Jong Dae
Issue Date
2021-10
Publisher
SPRINGERNATURE
Citation
CELL DEATH & DISEASE, v.12, no.11, pp.971
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.
URI
https://scholarworks.unist.ac.kr/handle/201301/54880
URL
https://www.nature.com/articles/s41419-021-04275-6
DOI
10.1038/s41419-021-04275-6
ISSN
2041-4889
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BIO_Journal Papers
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