ArticlePediatric rheumatology online journal2013
DC-SIGN gene promoter variants and IVIG treatment response in Kawasaki disease.
Article in Pediatric rheumatology online journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Intravenous Immunoglobulin in Kawasaki Disease-Evolution and Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2023Review
- Pharmacogenomics of intravenous immunoglobulin response in Kawasaki disease.Frontiers in immunology · 2023Article
- Systems biology and artificial intelligence analysis highlights the pleiotropic effect of IVIg therapy in autoimmune diseases with a predominant role on B cells and complement system.Frontiers in immunology · 2022Article
- Homozygous ofFrontiers in genetics · 2021Article
- Identification of SAMD9L as a susceptibility locus for intravenous immunoglobulin resistance in Kawasaki disease by genome-wide association analysis.The pharmacogenomics journal · 2020Article
- Infectivity and Progression of COVID-19 Based on Selected Host Candidate Gene Variants.Frontiers in genetics · 2020Article
- Association of Single-Nucleotide Polymorphisms in DC-SIGN with Nasopharyngeal Carcinoma Susceptibility.Disease markers · 2017Article
- Gene-Gene Associations with the Susceptibility of Kawasaki Disease and Coronary Artery Lesions.PloS one · 2015Article
- High-density genotyping of immune loci in Kawasaki disease and IVIG treatment response in European-American case-parent trio study.Genes and immunity · 2014Article
- Type I and type II Fc receptors regulate innate and adaptive immunity.Nature immunology · 2014Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenetic variants in the inhibiting FcγRIIB mediate anti-inflammatory responses and influence IVIG refractoriness (IVIG-R). However, these variants are rare in Asian and Hispanic populations so other genes in the pathway could be potentially involved. IVIG is ineffective in mice lacking SIGN-R1, a related molecule to human DC-SIGN. Further, DC-SIGN is a known receptor for sialylated Fc, the component responsible for the anti-inflammatory action of IVIG. Thus, we hypothesized that DC-SIGN would also be involved in the pathway of IVIG response in Kawasaki Disease (KD) patients.
findingsA case-control approach was performed to examine the differential distribution of five single nucleotide polymorphisms (SNPs) in DC-SIGN promoter with IVIG-R among White (158 vs. 62), Asian (64 vs. 12) and Hispanic (55 vs. 20) KD patients. Distinct differences in allele frequency distributions of several variants in the DC-SIGN promoter were observed in the three ethnic groups. Further, Asians with the major allele "A" in rs2287886 were more likely (OR = 1.76, p = 0.04) to be IVIG non-responder, but this allele is a minor allele in other two ethnic groups, where the association was not apparent.
conclusionsDC-SIGN can potentially complement the role of FcγRIIB in the anti-inflammatory cascade involved in the IVIG response mechanism.
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Registered trials
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.