Evidence map›Paper›PMID 41857650›Full record

ArticleArthritis research & therapy2026

Characteristics of CLA⁺Tregs in rheumatoid arthritis and their potential as biomarkers of treatment response.

Danxue Zhu, Feng Sun, Xi Zheng, Wenxin Cai, Ping Wang, Sitian Zang, Yingni Li, Xu Jin, Yuke Hou, Peishi Rao and 8 more

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Danxue Zhu *Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Feng Sun *Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Xi ZhengDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Wenxin CaiDepartment of Rheumatology and immunology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, 100730, PR China.
Ping WangDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Sitian ZangDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Yingni LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Xu JinDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Yuke HouDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Peishi RaoDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Yang XieDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Shuyan LiuDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Jiachen LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Yan WangDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Chaonan WeiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China.
Xiaolin SunDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China. sunxiaolin_sxl@126.com.
Fanlei HuDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China. fanleihu@bjmu.edu.cn.
Zhanguo LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis, Beijing, 100044, China. li99@bjmu.edu.cn.

Funding

National Natural Science Foundation of China 32441099National Natural Science Foundation of China 92374202Natural Science Foundation of Beijing Municipality 7252143
6 · The paper itself

Abstract

backgroundThe newly discovered Treg subset (CLA+ Tregs) expressing cutaneous lymphocyte-associated antigen is associated with inflammatory conditions. This study elucidated the role of CLA+ Tregs in rheumatoid arthritis (RA) development and its responses to treatment.

methodsA total of 12 T cell subsets, together with total T cells, B cells, and NK cells were analyzed in 169 patients with RA and 114 healthy controls using flow cytometry. Autoantibodies were detected by ELISA. The logistic regression models were employed to assess the association between cell subsets and rheumatoid arthritis. Relationships between CLA+ Tregs and clinical variables were assessed.

resultsAmong the immune cell subsets analyzed, CLA⁺ Tregs were the most significantly reduced ones in patients with RA compared with healthy controls (OR 0.825 [0.764–0.891], p < 0.001). Decreased CLA⁺ Tregs were strongly correlated to active disease status (adjusted OR 0.814 [0.733–0.902], p = 0.004; AUC 0.916 [0.869–0.963], p < 0.001). Decreased CLA+ Tregs were associated with higher swollen joint count, tender joint count and DAS28 scores, as well as systemic involvements, including interstitial lung disease (ILD), anemia, fever, and skin vasculitis. Additionally, rheumatoid factor (RF) and anti-mutated citrullinated vimentin antibody (anti-MCV) were correlated to lower CLA+ Tregs. Compared to baseline prior treatment, CLA+ Tregs increased significantly in RA patients, accompanied by improvements in disease activity (median, 9.60% vs. 18.80%, p = 0.044; 3.41 cells/µL vs. 7.86 cells/µL, p = 0.011, respectively).

conclusionsThe results demonstrated a significant reduction of CLA+ Tregs in active RA, especially in patients with systemic damages. Recovery of CLA+ Tregs may predict therapeutic responses.

Indexed as

Arthritis, RheumatoidT-Lymphocytes, RegulatoryAdultAgedAntirheumatic AgentsAutoantibodiesBiomarkersFemaleFlow CytometryHumansMaleMiddle AgedTreatment OutcomeAntirheumatic AgentsAutoantibodiesBiomarkersCLA+ TregsDisease activityRheumatoid arthritisTherapeutic responses

Identifiers

PMID41857650
PMCPMC13123160

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