Evidence map›Paper›PMID 35628531›Full record

ArticleInternational journal of molecular sciences2022

IL-17A Is the Critical Cytokine for Liver and Spleen Amyloidosis in Inflammatory Skin Disease.

Shohei Iida, Takehisa Nakanishi, Fumiyasu Momose, Masako Ichishi, Kento Mizutani, Yoshiaki Matsushima, Ai Umaoka, Makoto Kondo, Koji Habe, Yoshifumi Hirokawa and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. 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
2.2field-weighted citation impact, top 12% 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.

  1. Diffuse uptake in the subcutaneous tissue onEuropean journal of nuclear medicine and molecular imaging · 2026
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  6. Review
  7. [Mechanism of IL-17 Signaling Pathway in Spleen Inflammatory Response Induced by Altitude Hypoxia in Mice].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  8. Article
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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 2 institutions in 1 country.

Shohei IidaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Takehisa NakanishiDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Fumiyasu MomoseDepartment of Personalized Cancer Immunotherapy, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Masako IchishiDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Kento MizutaniDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.ORCID 0000-0001-5171-4909
Yoshiaki MatsushimaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.ORCID 0000-0001-6114-0830
Ai UmaokaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Makoto KondoDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Koji HabeDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Yoshifumi HirokawaDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Masatoshi WatanabeDepartment of Oncologic Pathology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Yoichiro IwakuraCenter for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.ORCID 0000-0002-9934-5775
Yoshihiro MiyaharaDepartment of Personalized Cancer Immunotherapy, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Yasutomo ImaiDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.ORCID 0000-0003-3169-5717
Keiichi YamanakaDepartment of Dermatology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan.
Mie University · JPTokyo University of Science · JP

Funding

AbbVie GK noneEli Lilly and Company noneSun Pharma noneThe Maruho Takagi Dermatology Foundation none
6 · The paper itself

Abstract

Systemic amyloidosis is recognized as a serious complication of rheumatoid arthritis or inflammatory bowel disease, but also of inflammatory skin disease. However, the detailed molecular mechanism of amyloidosis associated with cutaneous inflammation remains unclear, and therapeutic approaches are limited. Here, we investigated the pathophysiology of amyloidosis secondary to cutaneous inflammation and the therapeutic effects of Janus kinase (JAK) inhibitors by examining a mouse model of spontaneous dermatitis (KCASP1Tg mice). Moreover, KCASP1Tg mice were crossed with interleukin-17A (IL-17A) knockout mice to generate IL-17A-/KCASP1Tg and examine the role of IL-17A in amyloidosis under cutaneous inflammation. KCASP1Tg mice showed severe amyloid deposition in the liver and spleen. Increased serum-neutral fat levels and decreased lymphocyte production were observed in the spleen. Overproduction of amyloidosis was partially ameliorated by the administration of JAK inhibitors and was further improved in IL-17A-/KCASP1Tg mice. IL-17A-producing cells included CD4, gamma delta, and CD8 T cells. In summary, our results from the analysis of a mouse model of dermatitis revealed that skin-derived inflammatory cytokines can induce amyloid deposition in the liver and spleen, and that the administration of JAK inhibitors and, even more, IL-17A ablation, reduced amyloidosis. This study demonstrates that active control of skin inflammation is essential to prevent internal organ amyloidosis.

Indexed as

AmyloidosisDermatitis, AtopicInterleukin-17Janus Kinase InhibitorsSkin DiseasesAnimalsCytokinesDisease Models, AnimalInflammationLiverMiceSpleenCytokinesIl17a protein, mouseInterleukin-17Janus Kinase InhibitorsamyloidosiscytokinedermatitisIL-17Ainflammatory skinJAK inhibitormouse model

Identifiers

PMID35628531
PMCPMC9147816
OpenAlexW4280568855

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.