Evidence map›Paper›PMID 30169661›Full record

ArticleInternational immunology2019

Ficolin-1 is a promising therapeutic target for autoimmune diseases.

Michihito Katayama, Kaori Ota, Noriko Nagi-Miura, Naohito Ohno, Norikazu Yabuta, Hiroshi Nojima, Atsushi Kumanogoh, Toru Hirano

Abstract read
In one paragraph

Article in International immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Ficolin-1 in pediatricInfection and immunity · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Pattern recognition receptors in health and diseases.Signal transduction and targeted therapy · 2021
    Review
  19. Article
  20. Article
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

8 authors at 2 institutions in 1 country.

Michihito KatayamaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Kaori OtaDepartment of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Noriko Nagi-MiuraCenter for the Advancement of Pharmaceutical Education, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Horinouchi, Hachioji, Tokyo, Japan.
Naohito OhnoLaboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Horinouchi, Hachioji, Tokyo, Japan.
Norikazu YabutaDepartment of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Hiroshi NojimaDepartment of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Toru HiranoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Yamadaoka, Suita, Osaka, Japan.
Osaka University · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we reported that mRNA expression of ficolin-1 (FCN1), a component of the complement lectin pathway, is elevated in peripheral blood mononuclear cells of patients with vasculitis syndrome, and that FCN1-positive cells infiltrate into inflamed regions in patient specimens. In addition, we reported that the serum FCN1 concentration is elevated in patients with Kawasaki disease (KD), a pediatric vasculitis, but dramatically decreases after intravenous immunoglobulin (IVIG) treatment. Furthermore, we showed that FCN1 binds to IgG1 in a pull-down assay. These results suggested that removal of FCN1 may be a therapeutic mechanism of IVIG. In this study, we prepared anti-FCN1 monoclonal antibody (mAb) and examined its therapeutic potential in mice treated with Candida albicans water-soluble fraction (CAWS), which induces KD-like vasculitis in the coronary artery. Indeed, treatment with anti-FCN1 mAb decreased the histological score of vasculitis (P = 0.03). To investigate the role of FCN1, we assessed blood samples of patients with various autoimmune diseases and demonstrated that serum levels of FCN1 were elevated not only in patients with vasculitis, but also in those with rheumatoid arthritis. Additionally, FCN1-targeted treatment of a mouse model of arthritis [collagen antibody-induced arthritis (CAIA)] revealed that administration of anti-FCN1 mAb ameliorated symptoms of arthritis (P < 0.01). These results suggest that FCN1 is involved in the pathogenesis of autoimmune diseases, and that targeting FCN1 represents a promising strategy for treating these diseases.

Indexed as

AgedAnimalsAntibodies, MonoclonalArthritis, RheumatoidAutoimmune DiseasesBiomarkersComplement System ProteinsDisease Models, AnimalFemaleFicolinsHumansLectinsMaleMiceMiddle AgedMolecular Targeted TherapyAntibodies, MonoclonalBiomarkersComplement System ProteinsFicolinsLectins

Identifiers

PMID30169661
PMCPMC6364620
OpenAlexW2889397971

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.