Evidence map›Paper›PMID 37639581›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

CD45 alleviates airway inflammation and lung fibrosis by limiting expansion and activation of ILC2s.

Guangwei Cui, Akihiro Shimba, Jianshi Jin, Nozomi Hojo, Takuma Asahi, Shinya Abe, Aki Ejima, Shinri Okada, Keizo Ohira, Ryoma Kato and 5 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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

15 authors at 3 institutions in 1 country.

Guangwei Cui *Laboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Akihiro Shimba *Laboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Jianshi JinLaboratory for Prediction of Cell Systems Dynamics, RIKEN Center for Biosystems Dynamics Research, Osaka 565-0874, Japan.
Nozomi HojoLaboratory for Prediction of Cell Systems Dynamics, RIKEN Center for Biosystems Dynamics Research, Osaka 565-0874, Japan.ORCID 0000-0003-0641-5533
Takuma AsahiLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Shinya AbeLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Aki EjimaLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Shinri OkadaLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Keizo OhiraLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Ryoma KatoLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Shizue Tani-IchiLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Ryo YamadaCenter for Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.ORCID 0000-0002-1587-630X
Takashi EbiharaDepartment of Medical Biology, Graduate School of Medicine, Akita University, Akita 010-8543, Japan.ORCID 0000-0002-6056-3230
Katsuyuki ShiroguchiLaboratory for Prediction of Cell Systems Dynamics, RIKEN Center for Biosystems Dynamics Research, Osaka 565-0874, Japan.ORCID 0000-0003-4025-8789
Koichi IkutaLaboratory of Immune Regulation, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
Kyoto University · JPRIKEN Center for Biosystems Dynamics Research · JPAkita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group 2 innate lymphoid cells (ILC2s) are critical for the immune response against parasite infection and tissue homeostasis and involved in the pathogenesis of allergy and inflammatory diseases. Although multiple molecules positively regulating ILC2 development and activation have been extensively investigated, the factors limiting their population size and response remain poorly studied. Here, we found that CD45, a membrane-bound tyrosine phosphatase essential for T cell development, negatively regulated ILC2s in a cell-intrinsic manner. ILC2s in CD45-deficient mice exhibited enhanced proliferation and maturation in the bone marrow and hyperactivated phenotypes in the lung with high glycolytic capacity. Furthermore, CD45 signaling suppressed the type 2 inflammatory response by lung ILC2s and alleviated airway inflammation and pulmonary fibrosis. Finally, the interaction with galectin-9 influenced CD45 signaling in ILC2s. These results demonstrate that CD45 is a cell-intrinsic negative regulator of ILC2s and prevents lung inflammation and fibrosis via ILC2s.

Indexed as

Pulmonary FibrosisAnimalsImmunity, InnateInflammationLymphocytesMiceSignal Transductionairway inflammationCD45fibrosisinnate lymphoid cellmetabolism

Identifiers

PMID37639581
PMCPMC10483638
OpenAlexW4386211829

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.