Evidence map›Paper›PMID 41562059›Full record

ArticleFrontiers in immunology2025

Regnase-1 in cDC1 controls T cell priming and shapes the dynamics of experimental autoimmune encephalomyelitis.

Xingyu Rong, Hai Wang, Shintaro Muraoka, Takuya Uehata, Masanori Yoshinaga, Tsuneyasu Kaisho, Osamu Takeuchi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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.

Xingyu Rong *Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hai Wang *Key Laboratory of Breast Cancer in Shanghai, Department of Breast Surgery, Precision Cancer Medicine Center, Fudan University Shanghai Cancer Center, Shanghai, China.
Shintaro MuraokaDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takuya UehataDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masanori YoshinagaDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tsuneyasu KaishoIndustry-Government-Academia Collaboration Promotion Headquarters, Wakayama Medical University, Wakayama, Japan.
Osamu TakeuchiDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system (CNS), in which various immune cells contribute to disease progression, yet the role of dendritic cells (DCs) remains incompletely understood. The RNA-binding protein Regnase-1 plays an important role in regulating immune cell function, but its function in DCs, particularly conventional type 1 DCs (cDC1), has not been defined. Methods: We investigated the role of Regnase-1 in cDC1 and its impact on experimental autoimmune encephalomyelitis (EAE) on Results: Reduced Regnase-1 expression in cDC1 enhanced pro-inflammatory gene expression and increased their capacity to activate T cells. In the EAE model, Discussion: Our study reveals the complex role for cDC1 with reduced Regnase-1 expression in inflammatory regulation, exacerbating inflammatory responses during the acute phase, while facilitate recovery. This dual role highlights Regnase-1 in cDC1 as a critical regulator that balances inflammation and immune memory.

Indexed as

Dendritic CellsEncephalomyelitis, Autoimmune, ExperimentalRibonucleasesT-LymphocytesAnimalsFemaleLymphocyte ActivationMiceMice, Inbred C57BLRibonucleasesZc3h12a protein, mouseautoimmune diseaseconventional type I dendritic cellsinflammationpost-transcriptional regulationRegnase-1

Identifiers

PMID41562059
PMCPMC12812901

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.