Evidence map›Paper›PMID 35015026›Full record

ArticleThe Journal of experimental medicine2022

CD127 imprints functional heterogeneity to diversify monocyte responses in inflammatory diseases.

Bin Zhang, Yuan Zhang, Lei Xiong, Yuzhe Li, Yunliang Zhang, Jiuliang Zhao, Hui Jiang, Can Li, Yunqi Liu, Xindong Liu and 7 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 71 citations in OpenAlex.

  1. Integrated single-cell transcriptomic analysis identifiesBiochemistry and biophysics reports · 2026
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  6. Induction of dysfunctional CD14Frontiers in immunology · 2026
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  8. Airway Immune Signatures in Severe and Fatal Infection with COVID-19.American journal of respiratory cell and molecular biology · 2025
    Article
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  11. Article
  12. Article
  13. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 7 institutions in 1 country.

Bin Zhang *Institute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0001-6232-6768
Yuan Zhang *Institute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-3689-2560
Lei XiongMinistry of Education Key Laboratory of Bioinformatics, Beijing Advanced Innovation Center for Structural Biology, Center for Synthetic and Systems Biology, School of Life Sciences, Tsinghua University, Beijing, China.ORCID 0000-0002-2392-114X
Yuzhe LiAcademy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.ORCID 0000-0002-0170-8639
Yunliang ZhangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-3126-520X
Jiuliang ZhaoDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunological Diseases, Beijing, China.ORCID 0000-0001-9308-2858
Hui JiangDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunological Diseases, Beijing, China.ORCID 0000-0003-4405-7984
Can LiDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunological Diseases, Beijing, China.ORCID 0000-0002-0960-9942
Yunqi LiuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-1244-128X
Xindong LiuInstitute of Pathology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0002-2465-0337
Haofei LiuInstitute of Pathology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0002-4584-3103
Yi-Fang PingInstitute of Pathology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0002-0699-8401
Qiangfeng Cliff ZhangMinistry of Education Key Laboratory of Bioinformatics, Beijing Advanced Innovation Center for Structural Biology, Center for Synthetic and Systems Biology, School of Life Sciences, Tsinghua University, Beijing, China.ORCID 0000-0002-4913-0338
Zheng ZhangInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, Shenzhen, China.ORCID 0000-0002-3544-1389
Xiu-Wu BianInstitute of Pathology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0003-4383-0197
Yan ZhaoDepartment of Rheumatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunological Diseases, Beijing, China.
Xiaoyu HuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0002-4289-6998
Tsinghua University · CNArmy Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNBeijing Friendship Hospital · CNCenter for Life Sciences · CNPeking University · CNSouthern University of Science and Technology · CN

Funding

Chongqing Health Commission 2020NCPZX01Ministry of Science and Technology of the People's Republic of China 2020YFA0509100National Natural Science Foundation of China 31725010Tsinghua-Peking Center for Life SciencesTsinghua University COVID-19 Scientific Research Program 2020Z99CFZ024
6 · The paper itself

Abstract

Inflammatory monocytes are key mediators of acute and chronic inflammation; yet, their functional diversity remains obscure. Single-cell transcriptome analyses of human inflammatory monocytes from COVID-19 and rheumatoid arthritis patients revealed a subset of cells positive for CD127, an IL-7 receptor subunit, and such positivity rendered otherwise inert monocytes responsive to IL-7. Active IL-7 signaling engaged epigenetically coupled, STAT5-coordinated transcriptional programs to restrain inflammatory gene expression, resulting in inverse correlation between CD127 expression and inflammatory phenotypes in a seemingly homogeneous monocyte population. In COVID-19 and rheumatoid arthritis, CD127 marked a subset of monocytes/macrophages that retained hypoinflammatory phenotypes within the highly inflammatory tissue environments. Furthermore, generation of an integrated expression atlas revealed unified features of human inflammatory monocytes across different diseases and different tissues, exemplified by those of the CD127high subset. Overall, we phenotypically and molecularly characterized CD127-imprinted functional heterogeneity of human inflammatory monocytes with direct relevance for inflammatory diseases.

Indexed as

Arthritis, RheumatoidCOVID-19Epigenesis, GeneticFemaleHumansInflammationInterleukin-7Interleukin-7 Receptor alpha SubunitMaleMonocytesSARS-CoV-2IL7 protein, humanIL7R protein, humanInterleukin-7Interleukin-7 Receptor alpha Subunit

Identifiers

PMID35015026
PMCPMC8757045
OpenAlexW4206232024

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.