Evidence map›Paper›PMID 31570755›Full record

ArticleNature communications2019

Abl family tyrosine kinases govern IgG extravasation in the skin in a murine pemphigus model.

Sachiko Ono, Gyohei Egawa, Takashi Nomura, Akihiko Kitoh, Teruki Dainichi, Atsushi Otsuka, Saeko Nakajima, Masayuki Amagai, Fumi Matsumoto, Mami Yamamoto and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. 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
0.5field-weighted citation impact, top 34% 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, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

14 authors at 5 institutions in 2 countries.

Sachiko OnoDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Gyohei EgawaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. gyohei@kuhp.kyoto-u.ac.jp.
Takashi NomuraDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akihiko KitohDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Teruki DainichiDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-9497-0029
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Saeko NakajimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masayuki AmagaiDepartment of Dermatology, Keio University Graduate School of Medicine, Tokyo, Japan.
Fumi MatsumotoResearch Unit/Immunology & Inflammation, Sohyaku, Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Mami YamamotoResearch Unit/Immunology & Inflammation, Sohyaku, Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.ORCID http://orcid.org/0000-0002-3141-6290
Yoshiaki KubotaDepartment of Anatomy, Keio University School of Medicine, Tokyo, Japan.
Toshiyuki TakaiDepartment of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Tetsuya HondaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenji KabashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. kaba@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-0773-0554
Kyoto University · JPKeio University · JPMitsubishi Tanabe Pharma CorporationAgency for Science, Technology and Research · SGTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathway of homeostatic IgG extravasation is not fully understood, in spite of its importance for the maintenance of host immunity, the management of autoantibody-mediated disorders, and the use of antibody-based biologics. Here we show in a murine model of pemphigus, a prototypic cutaneous autoantibody-mediated disorder, that blood-circulating IgG extravasates into the skin in a time- and dose-dependent manner under homeostatic conditions. This IgG extravasation is unaffected by depletion of Fcγ receptors, but is largely attenuated by specific ablation of dynamin-dependent endocytic vesicle formation in blood endothelial cells (BECs). Among dynamin-dependent endocytic vesicles, IgG co-localizes well with caveolae in cultured BECs. An Abl family tyrosine kinase inhibitor imatinib, which reduces caveolae-mediated endocytosis, impairs IgG extravasation in the skin and attenuates the murine pemphigus manifestations. Our study highlights the kinetics of IgG extravasation in vivo, which might be a clue to understand the pathological mechanism of autoantibody-mediated autoimmune disorders.

Indexed as

AnimalsAutoantibodiesAutoimmune DiseasesCaveolaeDisease Models, AnimalDynaminsEarEndocytosisEndothelial CellsFemaleImmunoglobulin GKineticsMiceMice, Inbred C57BLPemphigusProtein-Tyrosine KinasesAutoantibodiesDynaminsImmunoglobulin GProtein-Tyrosine Kinases

Identifiers

PMID31570755
PMCPMC6769004
OpenAlexW2975942999

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.