Evidence map›Paper›PMID 40374622›Full record

ArticleNature communications2025

TIGIT deficiency promotes autoreactive CD4

Yimei Lai, Shuang Wang, Tingting Ren, Jia Shi, Yichao Qian, Shuyi Wang, Mianjing Zhou, Ryu Watanabe, Mengyuan Li, Xinyuan Ruan and 6 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

16 authors.

Yimei Lai *Department of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shuang Wang *Department of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Tingting Ren *Department of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.ORCID http://orcid.org/0009-0002-7555-3411
Jia ShiDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yichao QianDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Shuyi WangDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Mianjing ZhouDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Ryu WatanabeDepartment of Clinical Immunology, Osaka Metropolitan University Graduate School of Medicine, Osaka, Japan.
Mengyuan LiDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xinyuan RuanDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xin WangDepartment of Pediatrics, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Lili ZhuangDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zunfu KeInstitute of Precision Medicine, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Niansheng YangDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yuefang HuangDepartment of Pediatrics, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Hui ZhangDepartment of Rheumatology and Clinical immunology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. zhangh656@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-9692-3026

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071819National Natural Science Foundation of China (National Science Foundation of China) 82402113National Natural Science Foundation of China (National Science Foundation of China) 82471764National Natural Science Foundation of China (National Science Foundation of China) 92474103
6 · The paper itself

Abstract

Polymyositis (PM) is a systemic autoimmune disease characterized by muscular inflammatory infiltrates and degeneration. T-cell immunoreceptor with Ig and ITIM domains (TIGIT) contributes to immune tolerance by inhibiting T cell-mediated autoimmunity. Here, we show that a reduced expression of TIGIT in CD4

Indexed as

Autoimmune DiseasesCD4-Positive T-LymphocytesEpigenesis, GeneticReceptors, ImmunologicAcetylationAnimalsAutoimmunityCD28 AntigensCell DifferentiationDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutCD28 AntigensProto-Oncogene Proteins c-aktReceptors, ImmunologicT cell Ig and ITIM domain protein, mouseTIGIT protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID40374622
PMCPMC12081758

What OpenQuestion holds

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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.