Evidence map›Paper›PMID 33246326›Full record

ArticleRheumatology (Oxford, England)2021

Monocytic MDSCs skew Th17 cells toward a pro-osteoclastogenic phenotype and potentiate bone erosion in rheumatoid arthritis.

Shixian Chen, Chunqing Guo, Ran Wang, Zhitao Feng, Zheng Liu, Lisheng Wu, Di Zhao, Songyuan Zheng, Feilong Chen, Dingding Zhang and 7 more

Open access · greenAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Myeloid-Derived Suppressor Cells in Inflammatory Arthritis.International journal of molecular sciences · 2026
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  15. Fu-zi decoction attenuate rheumatoid arthritisFrontiers in pharmacology · 2024
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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

17 authors at 5 institutions in 2 countries.

Shixian ChenDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Chunqing GuoDepartment of Human & Molecular Genetics.
Ran WangDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Zhitao FengDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Zheng LiuDepartment of Human & Molecular Genetics.
Lisheng WuDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Di ZhaoDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Songyuan ZhengDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Feilong ChenDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Dingding ZhangDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Juan XuDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Junqing ZhuDepartment of Rheumatic & TCM Medical Center, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0003-4642-2981
Xiaoguang ChenGuangdong Provincial Key Laboratory of Tropical Disease Research, Department of Pathogen Biology, Southern Medical University School of Public Health, Guangzhou.
Zhanguo LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, China.
Christopher M WiseDepartment of Internal Medicine, Virginia Commonwealth University Medical Center.
Juan LiDepartment of Traditional Chinese Internal Medicine, School of Traditional Chinese Medicine.
Xiang-Yang WangDepartment of Human & Molecular Genetics.ORCID 0000-0003-2421-5367
Nanfang Hospital · CNVirginia Commonwealth University · USPeking University · CNSouthern Medical University · CNVirginia Commonwealth University Medical Center · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Kim Felder Rhoads · 1985 to 2026
$51.0M
Innate Pattern Recognition Receptor and Acetaminophen-induced Liver InjuryI01BX003275 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI Xiang-Yang Shawn Wang · 2019 to 2026
–
BLRD VA I01 BX003275NCI NIH HHS P30 CA016059
6 · The paper itself

Abstract

objectivesWhile myeloid-derived suppressor cells (MDSCs) were previously shown to promote a proinflammatory T helper (Th) 17 response in autoimmune conditions, a potential impact of the MDSC-Th17 immune axis on abnormal bone destruction in RA remains largely unknown.

methodsWe investigated the correlation between the frequency of MDSCs or its subsets and joint destruction in RA patients. The reciprocal actions of patient-derived MDSCs and Th17 cells were studied using osteoclast (OC) differentiation and bone resorption assays in vitro, which were further validated using mouse models of RA. Contribution of MDSCs to osteoclastogenesis and bone erosion in vivo was determined by depletion or transfer of MDSCs.

resultsHuman MDSCs, particularly monocytic MDSCs (M-MDSCs), exhibit inherent OC-differentiating capacity and positively correlate with clinical bone erosion in RA patients. Strikingly, patient-derived M-MDSCs can program Th17 cells towards a pro-osteoclastogenic phenotype, which in return potentiates OC differentiation via the receptor activator of nuclear factor κΒ ligand (RANK-L)-RANK signalling. This enhanced osteolysis driven by the reciprocal actions of M-MDSCs and Th17 cells is further confirmed using mouse models of RA. Selective depletion of M-MDSCs significantly ameliorates osteoclastogenesis and disease severity in arthritic mice, whereas transfer of M-MDSCs aggravates bone erosion associated with increased OCs in recipient mice.

conclusionOur findings highlight the functional plasticity of MDSCs and identify a novel pro-osteoclastogenic pathway governed by interplay between myeloid cells and T lymphocytes in autoimmune RA.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidBone ResorptionCell DifferentiationHumansMiceMonocytesMyeloid-Derived Suppressor CellsOsteoclastsPhenotypeTh17 Cellsbone erosionmyeloid-derived suppressor cellosteoclastrheumatoid arthritisTh17

Identifiers

PMID33246326
PMCPMC8121448
OpenAlexW3107938469

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.