Evidence map›Paper›PMID 36288286›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Up-regulation of BTN3A1 on CD14

Jiaqing Zhou, Jingjing Zhang, Lu Tao, Kexin Peng, Qiaoan Zhang, Kexiang Yan, Jing Luan, Jiewen Pan, Xiaohui Su, Jiping Sun and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
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  15. Review
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  17. Article
  18. Reply to Herrmann et al.: The BTN3A isoform BTN3A1 is responsible for phosphoantigen-induced Vγ9Vδ2 T cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Caveat: Monoclonal antibodies 20.1 and 103.2 bind all human BTN3A proteins and are not suited to study BTN3A1-specific features.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Mechanisms and Applications of γδ T Cells in Anti-Tumor Immunity.Cancer control : journal of the Moffitt Cancer Center
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Jiaqing ZhouDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Jingjing ZhangShanghai Institute of Immunology, Department of Immunology and Microbiology, and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-4707-415X
Lu TaoDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Kexin PengDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Qiaoan ZhangDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Kexiang YanDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Jing LuanDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Jiewen PanDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.
Xiaohui SuShanghai Institute of Immunology, Department of Immunology and Microbiology, and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jiping SunShanghai Institute of Immunology, Department of Immunology and Microbiology, and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Zhenghua ZhangDepartment of Dermatology, Huashan Hospital, Shanghai Medical College of Fudan University, Shanghai 200040, China.ORCID 0000-0001-9335-7022
Lei ShenShanghai Institute of Immunology, Department of Immunology and Microbiology, and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Shanghai Medical College of Fudan University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vγ9Vδ2 T cells play an important role in the development and progression of psoriasis vulgaris (PV), but how they promote skin inflammation and the molecular mechanisms underlying Vγ9Vδ2 T cell dysfunction are poorly understood. Here, we show that circulating Vγ9Vδ2 T cells are decreased and exhibit enhanced proliferation and increased production of IFN-γ and TNF-α in PV patients. Monocytes from PV patients express higher levels of the phosphoantigen sensor butyrophilin 3A1 (BTN3A1) than monocytes from healthy controls. Blockade of BTN3A1 suppresses Vγ9Vδ2 T cell activation and abolishes the difference in Vγ9Vδ2 T cell activation between PV patients and healthy controls. The CD14

Indexed as

PsoriasisReceptors, Antigen, T-Cell, gamma-deltaAntigensAntigens, CDButyrophilinsHumansLymphocyte ActivationT-LymphocytesTumor Necrosis Factor-alphaUp-RegulationAntigensAntigens, CDBTN3A1 protein, humanButyrophilinsReceptors, Antigen, T-Cell, gamma-deltaTumor Necrosis Factor-alphaBTN3A1monocytespsoriasisVγ9Vδ2 T cells

Identifiers

PMID36288286
PMCPMC9636952
OpenAlexW4307309275

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.