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ScientificWorldJournal. 2012;2012:634835. doi: 10.1100/2012/634835. Epub 2012 May 2.

DC-SIGN (CD209) promoter -336 A/G (rs4804803) polymorphism associated with susceptibility of Kawasaki disease.

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1
Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan.

Abstract

Kawasaki disease (KD) is characterized by systemic vasculitis of unknown etiology. High-dose intravenous immunoglobulin (IVIG) is the most effective therapy for KD to reduce the prevalence of coronary artery lesion (CAL) formation. Recently, the α2, 6 sialylated IgG was reported to interact with a lectin receptor, specific intracellular adhesion molecule-3 grabbing nonintegrin homolog-related 1 (SIGN-R1) in mice and dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) in human, and to trigger an anti-inflammatory cascade. This study was conducted to investigate whether the polymorphism of DC-SIGN (CD209) promoter -336 A/G (rs4804803) is responsible for susceptibility and CAL formation in KD patients using Custom TaqMan SNP Genotyping Assays. A total of 521 subjects (278 KD patients and 243 controls) were investigated to identify an SNP of rs4804803, and they were studied and showed a significant association between the genotypes and allele frequency of rs4804803 in control subjects and KD patients (P = 0.004 under the dominant model). However, the promoter variant of DC-SIGN gene was not associated with the occurrence of IVIG resistance, CAL formation in KD. The G allele of DC-SIGN promoter -336 (rs4804803) is a risk allele in the development of KD.

PMID:
22629172
PMCID:
PMC3354554
DOI:
10.1100/2012/634835
[Indexed for MEDLINE]
Free PMC Article
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