Evidence map›Paper›PMID 34671026›Full record

ArticleCell death & disease2021

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

Younseo Oh, Robin Park, So Yeon Kim, Sung-Ho Park, Sungsin Jo, Tae-Hwan Kim, Jong Dae Ji

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

Younseo OhHanyang University Institute for Rheumatology Research, Seoul, Republic of Korea.
Robin ParkMetroWest Medical Center/Tufts University School of Medicine, Framingham, MA, 01702, USA.
So Yeon KimHanyang University Institute for Rheumatology Research, Seoul, Republic of Korea.
Sung-Ho ParkSchool of Life Sciences, Ulsan National Institute of Science & Technology (UNIST), Ulsan, 44919, Korea.
Sungsin JoHanyang University Institute for Rheumatology Research, Seoul, Republic of Korea.
Tae-Hwan KimHanyang University Institute for Rheumatology Research, Seoul, Republic of Korea. thkim@hanyang.ac.kr.ORCID 0000-0002-3542-2276
Jong Dae JiRheumatology, College of Medicine, Korea University, Seoul, South Korea. jjdjmesy@korea.ac.kr.ORCID 0000-0002-9772-1992
Hanyang University · KRKorea University · KRHanyang University Seoul Hospital · KRTufts University · USUlsan National Institute of Science and Technology · KR

Funding

National Research Foundation of Korea (NRF) 2019R1A2C1083857National Research Foundation of Korea (NRF) 2021R1A6A1A03038899
6 · The paper itself

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.

Indexed as

Cell DifferentiationAnimalsAntibodies, NeutralizingArthritis, RheumatoidB7 AntigensEnzyme InductionHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-betaInterferon Type IMacrophage Colony-Stimulating FactorMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutAntibodies, NeutralizingB7 AntigensCD276 protein, humanCd276 protein, mouseIDO1 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-betaInterferon Type IMacrophage Colony-Stimulating FactorNitric Oxide Synthase Type IIProto-Oncogene Proteins c-fosRNA, MessengerSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinTryptophan

Identifiers

PMID34671026
PMCPMC8528854
OpenAlexW3206224802

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.