Evidence map›Paper›PMID 42503518›Full record

ArticleInternational journal of oral science2026

Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis.

Jiawei Lu, Xiao Wu, Zehui Xiong, Jinyi Zhang, Haipeng Yang, Feng Liu, Lijun Luo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oral science, 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

7 authors.

Jiawei Lu *Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Xiao Wu *Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Zehui XiongShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Jinyi ZhangShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Haipeng YangShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Feng LiuShanghai Key Laboratory of Sleep Disordered Breathing, Otolaryngology Institute of Shanghai Jiao Tong University, Department of Otolaryngology-Head and Neck Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. liufeng@sibs.ac.cn.ORCID http://orcid.org/0000-0002-4442-7028
Lijun LuoShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China. juneluo@yeah.net.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82071123
6 · The paper itself

Abstract

Lymphocytes play a central role in adaptive immunity and represent the primary source of RANKL in periodontitis. Understanding their organization and activation within gingiva is therefore essential. This study investigates the role of tertiary lymphoid structures (TLSs), ectopic lymphoid aggregates that orchestrate local immune responses. Using multiplex immunohistochemistry staining, we found that TLSs form and mature with increasing inflammatory severity. These structures function as hubs for B cell activation and were associated with poorer surgical outcomes. Given the known role of fibroblasts in initiating TLS assembly, we explored the underlying mechanism. Using single-cell RNA sequencing and in vitro assays, we identified that oral pathogens activate the IFN-I-IRF7 axis in gingival fibroblasts, leading to overproduction of IFNβ and driving their differentiation into a CXCL13-producing subtype that facilitates TLS organization. Furthermore, in a mouse periodontitis model, we demonstrated that activated IgD

Indexed as

Alveolar Bone LossB-LymphocytesInterferon Type IPeriodontitisTertiary Lymphoid StructuresAnimalsDisease Models, AnimalFibroblastsHumansImmunohistochemistryMiceMice, Inbred C57BLRANK LigandInterferon Type IRANK Ligand

Identifiers

PMID42503518
PMCPMC13402716

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.