Evidence map›Paper›PMID 42256301›Full record

ArticleiScience2026

DCIR-mediated inhibitory regulation of TLR7-MyD88 axis prevents autoimmune neuroinflammation.

Atsushi Fujioka, Kenji Shimizu, Saki Nakayama, Dai Ueno, Yuki Chiba, Ichiro Nakashima, Juichi Fujimori, Yuko Shirota, Yoichiro Iwakura, Yasushi Muraki and 2 more

Abstract read
In one paragraph

Article in iScience, 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

12 authors.

Atsushi FujiokaDivision of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Kenji ShimizuLaboratory of Molecular Immunology, Institute for Quantitative Biosciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Saki NakayamaDivision of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Dai UenoDivision of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Yuki ChibaDivision of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Ichiro NakashimaDivision of Neurology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Juichi FujimoriDivision of Neurology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Yuko ShirotaDivision of Hematology and Rheumatology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Yoichiro IwakuraResearch Institute for Biomedical Sciences, Tokyo University of Science, 2669 Yamazaki, Noda, Chiba 278-0022, Japan.
Yasushi MurakiDivision of Infectious Disease and Immunology, Department of Microbiology, School of Medicine, Iwate Medical University, 1-1-1 Idaidori, Yahaba, Iwate 028-3694, Japan.
Akira NakamuraDivision of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, 1-15-1, Fukumuro, Miyagino, Sendai 983-8536, Japan.
Tomonori KaifuDivision of Infectious Disease and Immunology, Department of Microbiology, School of Medicine, Iwate Medical University, 1-1-1 Idaidori, Yahaba, Iwate 028-3694, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Encephalitogenic T cells are responsible for developing autoimmune diseases in the central nervous system (CNS), but the pathogenesis of CNS autoimmune diseases remains incompletely understood. Dendritic cell immunoreceptor (DCIR) is an inhibitory type of C-type lectin receptor that regulates the antigen presentation ability of DCs, and DCIR deficiency exacerbates autoimmune diseases. Here, we demonstrated that DCIR deficiency induced spontaneous development of experimental autoimmune encephalomyelitis (EAE)-like encephalomyelitis in 2D2 TCR transgenic mice (2D2Tg) expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell receptor. 2D2Tg

Indexed as

biological sciencesimmunologymolecular biology

Identifiers

PMID42256301
PMCPMC13241762

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.