Evidence map›Paper›PMID 42508033›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026

Polymorphonuclear Myeloid-Derived Suppressor Cells Promote Rheumatoid Arthritis by Inducing Age-Associated B Cells Proliferation and Differentiation via the BAFF-Mediated SYK-ERK1/2 Pathway.

Huiming Hong, Yanan Wang, Shuping Yan, Fanzhang Yin, Yongqi Wang, Jingxue Zhang, Xiaojun Tang, Mei Li, Huayong Zhang, Lingyun Sun

Abstract read
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In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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

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

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

10 authors.

Huiming HongDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Yanan WangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Shuping YanDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Fanzhang YinDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Yongqi WangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Jingxue ZhangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing Normal University, Nanjing, Jiangsu, People's Republic of China.
Xiaojun TangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing Normal University, Nanjing, Jiangsu, People's Republic of China.
Mei LiDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, People's Republic of China.ORCID https://orcid.org/0000-0001-9273-8237
Huayong ZhangDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Lingyun SunDepartment of Rheumatology and Immunology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, People's Republic of China.

Funding

MOST | National Natural Science Foundation of China (NSFC) 81671608MOST | National Natural Science Foundation of China (NSFC) 81971525
6 · The paper itself

Abstract

In rheumatoid arthritis (RA), there is a marked elevation of both polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) and age-associated B cells (ABCs) within affected joints, which are closely associated with the progression of disease. However, the interactions between these cell types remain poorly understood. This study seeks to elucidate the regulatory influence of PMN-MDSCs on ABCs and to uncover the underlying mechanisms, thereby providing novel insights into the pathogenesis of RA and identifying potential therapeutic targets. We observed increased frequencies of both PMN-MDSCs and ABCs in the joints and spleens of collagen-induced arthritis (CIA) mouse model, with a strong positive correlation specifically in joint tissues. RNA sequencing of CD11c

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidB-Cell Activating FactorB-LymphocytesCell DifferentiationMAP Kinase Signaling SystemMyeloid-Derived Suppressor CellsSyk KinaseAnimalsCell ProliferationMaleMiceMice, Inbred DBAMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3B-Cell Activating FactorMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Syk KinaseSyk protein, mouseTnfsf13b protein, mouseage‐associated B cellsB‐cell activating factorcollagen‐induced arthritispolymorphonuclear myeloid‐derived suppressor cellsrheumatoid arthritis

Identifiers

PMID42508033
PMCPMC13405864

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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.