ArticleScientific reports2017
FCN1 (M-ficolin), which directly associates with immunoglobulin G1, is a molecular target of intravenous immunoglobulin therapy for Kawasaki disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- The Etiopathogenesis of Kawasaki Disease: Evolving Understanding of Diverse Triggers.Immunity, inflammation and disease · 2025Review
- Multi-omics evaluation of the prognostic value and immune signature of FCN1 in pan-cancer and its relationship with proliferation and apoptosis in acute myeloid leukemia.Frontiers in genetics · 2024Article
- Intravenous Immunoglobulin in Kawasaki Disease-Evolution and Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2023Review
- Single-Cell RNA-Sequencing Atlas Reveals the Tumor Microenvironment of Metastatic High-Grade Serous Ovarian Carcinoma.Frontiers in immunology · 2022Article
- Complement 3 and the Prognostic Nutritional Index Distinguish Kawasaki Disease from Other Fever Illness with a Nomogram.Children (Basel, Switzerland) · 2021Article
- Single-cell RNA sequencing of peripheral blood mononuclear cells from acute Kawasaki disease patients.Nature communications · 2021Article
- The up-to-date pathophysiology of Kawasaki disease.Clinical & translational immunology · 2021Review
- Does the Lectin Complement Pathway Link Kawasaki Disease and SARS-CoV-2?Frontiers in immunology · 2020Article
- Ficolin-1 is a promising therapeutic target for autoimmune diseases.International immunology · 2019Article
- Aetiological Significance of Infectious Stimuli in Kawasaki Disease.Frontiers in pediatrics · 2019Review
- Isolation of cancer cells with augmented spheroid-forming capability using a novel tool equipped with removable filter.Oncotarget · 2018Article
- Serum exosomal miR-328, miR-575, miR-134 and miR-671-5p as potential biomarkers for the diagnosis of Kawasaki disease and the prediction of therapeutic outcomes of intravenous immunoglobulin therapy.Experimental and therapeutic medicine · 2018Article
- Late cornified envelope 1C (LCE1C), a transcriptional target of TAp63 phosphorylated at T46/T281, interacts with PRMT5.Scientific reports · 2018Article
- Sickening or Healing the Heart? The Association of Ficolin-1 and Rheumatic Fever.Frontiers in immunology · 2018Observational
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD), an acute systemic vasculitis of early childhood, is of unknown etiology. High-dose intravenous immunoglobulin (IVIG) is an effective treatment, but its molecular target remains elusive. DNA microarray analysis of peripheral blood mononuclear cells (PBMCs) revealed that at least 21 genes are drastically down-regulated after IVIG treatment in most KD patients. qRT-PCR analysis confirmed that the mRNA levels of five of these genes were considerably reduced in almost all KD patients after IVIG treatment. Western blot (Wb) of PBMC extracts revealed that levels of FCN1 (M-ficolin), a protein of the complement system that defends against infectious agents, were reduced after IVIG treatment in many KD patients. In another set of KD patients, Wb confirmed that levels of both FCN1 were greatly reduced after IVIG therapy. Wb revealed that the collagen-like domain of FCN1 directly bound to IgG1 in vitro through a portion of the CH1 and CH3 domains, and synthetic peptides corresponding to these domains of IgG1 efficiently inhibited these associations. These results suggest that FCN1 is a molecular target of intravenous IVIG in KD patients. We propose that these peptides and a humanized monoclonal antibody against FCN1 could be useful in combination therapy with IVIG.
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