Evidence map›Paper›PMID 40140451›Full record

ArticleScientific reports2025

Gingipain regulates isoform switches of PD-L1 in macrophages infected with Porphyromonas gingivalis.

Yilin Zheng, Ziyi Wang, Yao Weng, Heriati Sitosari, Yuhan He, Xiu Zhang, Noriko Shiotsu, Yoko Fukuhara, Mika Ikegame, Hirohiko Okamura

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Highly Alkaline-ResistantMicroorganisms · 2025
    Article
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.

Yilin Zheng *Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Ziyi Wang *Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8525, Japan.
Yao WengDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Heriati SitosariDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Yuhan HeDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Xiu ZhangDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Noriko ShiotsuComprehensive Dental Clinic, Okayama University Hospital, Okayama University, Okayama, 700-8525, Japan.
Yoko FukuharaDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Mika IkegameDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan.
Hirohiko OkamuraDepartment of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University, 2-5-1 Shikatacho, Kita-ku, Okayama, 700-8525, Japan. hiro-okamura@okayama-u.ac.jp.

Funding

Ministry of Education, Science, Sports, and Culture of Japan 21K19644Ministry of Education, Science, Sports, and Culture of Japan 22H03511Ministry of Education, Science, Sports, and Culture of Japan 22H06790Ministry of Education, Science, Sports, and Culture of Japan 23K18431
6 · The paper itself

Abstract

Periodontal pathogen Porphyromonas gingivalis (P. gingivalis) is believed to possess immune evasion capabilities, but it remains unclear whether this immune evasion is related to host gene alternative splicing (AS). In this study, RNA-sequencing revealed significant changes in both AS landscape and transcriptomic profile of macrophages following P. gingivalis infection with/without knockout of gingipain (a unique toxic protease of P. gingivalis). P. gingivalis infection increased the PD-L1 transcripts expression and selectively upregulated a specific coding isoform that more effectively binds to PD-1 on T cells, thereby inhibiting immune function. Biological experiments also detected AS switch of PD-L1 in P. gingivalis-infected or gingipain-treated macrophages. AlphaFold 3 predictions indicated that the protein docking compatibility between PD-1 and P. gingivalis-upregulated PD-L1 isoform was over 80% higher than another coding isoform. These findings suggest that P. gingivalis employs gingipain to modulate the AS of PD-L1, facilitating immune evasion.

Indexed as

B7-H1 AntigenBacteroidaceae InfectionsGingipain Cysteine EndopeptidasesMacrophagesPorphyromonas gingivalisAlternative SplicingAnimalsHost-Pathogen InteractionsHumansImmune EvasionMiceProtein IsoformsB7-H1 AntigenCD274 protein, humanGingipain Cysteine EndopeptidasesProtein IsoformsAlternative splicingGingipainImmune evasionMacrophagePD-L1Porphyromonas gingivalis

Identifiers

PMID40140451
PMCPMC11947232

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.