Evidence map›Paper›PMID 41438053›Full record

ArticleiScience2025

TLR9 decreases FOXO3 expression to prevent excessive inflammation in macrophage activation syndrome.

Mengyan Wang, Yuning Ma, Jianfen Meng, Chengde Yang, Dehao Zhu, Xia Chen, Longfang Chen, Yu Xiao, Da Yi, Hui Shi and 13 more

Abstract read
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In one paragraph

Article in iScience, 2025. 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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0cells of the map it votes in
0citing 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

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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

23 authors.

Mengyan WangDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yuning MaDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jianfen MengDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Chengde YangDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Dehao ZhuDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xia ChenDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Longfang ChenDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yu XiaoDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Da YiDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Hui ShiDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yue SunDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Honglei LiuDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xiaobing ChengDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yutong SuDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Junna YeDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Huihui ChiDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Zhuochao ZhouDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Tingting LiuDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Fan WangDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jialin TengDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ping HuGuangzhou Laboratory, Guangzhou International Bio Island, No. 9 XingDaoHuan Road, Guangzhou 510005, China.
Jinchao JiaDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Qiongyi HuDepartment of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult-onset Still's disease (AOSD) is characterized by an overwhelming inflammatory response and hyperactivation of monocytes/macrophages, which may cause macrophage activation syndrome (MAS). Here, we demonstrate the forkhead box protein O3 (FOXO3), a transcriptional factor downregulated by interferon, as an important regulator of inflammation in AOSD-MAS. FOXO3 expression is downregulated in monocytes/PBMCs from patients with AOSD, especially in those developing MAS. A negative correlation between FOXO3 expression with disease activity and inflammatory level is identified. FOXO3 downregulation can be induced by TLR9 activation both in the murine MAS model and TLR9 agonist-stimulated macrophages

Indexed as

biochemistrycell biologyimmunology

Identifiers

PMID41438053
PMCPMC12719771

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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.