Evidence map›Paper›PMID 33661938›Full record

ArticlePloS one2021

The pronounced lung lesions developing in LATY136F knock-in mice mimic human IgG4-related lung disease.

Yuko Waseda, Kazunori Yamada, Keishi Mizuguchi, Kiyoaki Ito, Satoshi Watanabe, Masahiko Zuka, Tamotsu Ishizuka, Marie Malissen, Bernard Malissen, Mitsuhiro Kawano and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

5 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

11 authors at 4 institutions in 2 countries.

Yuko WasedaThird Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Eiheiji, Fukui, Japan.ORCID 0000-0002-7120-8517
Kazunori YamadaDepartment of Rheumatology, Kanazawa University Hospital, Kanazawa, Japan.
Keishi MizuguchiDepartment of Diagnostic Pathology, Kanazawa University Hospital, Kanazawa, Japan.
Kiyoaki ItoDepartment of Rheumatology, Kanazawa University Hospital, Kanazawa, Japan.
Satoshi WatanabeDepartment oh Respiratory Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Masahiko ZukaDepartment of Forensic Medicine and Pathology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Tamotsu IshizukaThird Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Eiheiji, Fukui, Japan.
Marie MalissenCentre d'Immunologie de Marseille-Luminy, Aix Marseille Universite´, INSERM, CNRS, Marseille, France.
Bernard MalissenCentre d'Immunologie de Marseille-Luminy, Aix Marseille Universite´, INSERM, CNRS, Marseille, France.
Mitsuhiro KawanoDepartment of Rheumatology, Kanazawa University Hospital, Kanazawa, Japan.
Shoko MatsuiHealth Administration Center, University of Toyama, Toyama, Japan.ORCID 0000-0002-1328-5768
Kanazawa University · JPCentre National de la Recherche Scientifique · FRUniversity of Fukui · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleImmunoglobulin (Ig) G4-related disease (IgG4-RD) is a novel clinical disease entity characterized by an elevated serum IgG4 concentration and tumefaction or tissue infiltration by IgG4-positive plasma cells. Pathological changes are most frequently seen in the pancreas, lacrimal glands, and salivary glands, but pathological changes in the lung also exist. Linker for activation of T cell (LAT)Y136F knock-in mice show Th2-dominant immunoreactions with elevated serum IgG1 levels, corresponding to human IgG4. We have reported that LATY136F knock-in mice display several characteristic features of IgG4-RD and concluded that they constitute an appropriate model of human IgG4-RD in salivary glands, pancreas, and kidney lesions.

objectivesThe aim of this study is to evaluate whether lung lesions in LATY136F knock-in mice can be a model of IgG4-related lung disease.

methodsLung tissue samples from LATY136F knock-in mice (LAT) and wild-type mice (WT) were immunostained for IgG1 and obtained for pathological evaluation, and cell fractions and cytokine levels in broncho-alveolar lavage fluid (BALF) were analyzed.

resultsIn the LAT group, IgG1-positive inflammatory cells increased starting at 4 weeks of age and peaked at 10 weeks of age. The total cell count and percentage of lymphocytes increased significantly in BALF in the LAT group compared to the WT group. In BALF, Th2-dominant cytokines and transforming growth factor-β were also increased. In the LAT group, marked inflammation around broncho-vascular bundles peaked at 10 weeks of age. After 10 weeks, fibrosis around broncho-vascular bundles and bronchiectasis were observed in LATY136F knock-in mice but not WT mice.

conclusionsLATY136F knock-in mice constitute an appropriate model of lung lesions in IgG4-RD.

Indexed as

Adaptor Proteins, Signal TransducingImmunoglobulin G4-Related DiseaseLung DiseasesMembrane ProteinsMutation, MissenseAmino Acid SubstitutionAnimalsDisease Models, AnimalMiceMice, TransgenicAdaptor Proteins, Signal TransducingLat protein, mouseMembrane Proteins

Identifiers

PMID33661938
PMCPMC7932159
OpenAlexW3135142584

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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.