Genetic variants of CD209 associated with Kawasaki disease susceptibility

PLoS One. 2014 Aug 22;9(8):e105236. doi: 10.1371/journal.pone.0105236. eCollection 2014.

Abstract

Background: Kawasaki disease (KD) is a systemic vasculitis with unknown etiology mainly affecting children in Asian countries. Dendritic cell-specific intercellular adhesion molecule-3 grabbing non-integrin (DC-SIGN, CD209) in humans was showed to trigger an anti-inflammatory cascade and associated with KD susceptibility. This study was conducted to investigate the association between genetic polymorphisms of CD209 and the risk KD.

Methods: A total of 948 subjects (381 KD and 567 controls) were recruited. Nine tagging SNPs (rs8112310, rs4804800, rs11465421, rs1544766, rs4804801, rs2287886, rs735239, rs735240, rs4804804) were selected for TaqMan allelic discrimination assay. Clinical phenotypes, coronary artery lesions (CAL) and intravenous immunoglobulin (IVIG) treatment outcomes were collected for analysis.

Results: Significant associations were found between CD209 polymorphisms (rs4804800, rs2287886, rs735240) and the risk of KD. Haplotype analysis for CD209 polymorphisms showed that A/A/G haplotype (P = 0.0002, OR = 1.61) and G/A/G haplotype (P = 0.0365, OR = 1.52) had higher risk of KD as compared with G/G/A haplotype in rs2287886/rs735239/rs735240 pairwise allele analysis. There were no significant association in KD with regards to CAL formation and IVIG treatment responses.

Conclusion: CD209 polymorphisms were responsible for the susceptibility of KD, but not CAL formation and IVIG treatment responsiveness.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Case-Control Studies
  • Cell Adhesion Molecules / genetics*
  • Coronary Artery Disease / genetics
  • Coronary Artery Disease / pathology
  • Gene Frequency
  • Genetic Association Studies*
  • Genetic Predisposition to Disease*
  • Genetic Variation*
  • Genotype
  • Haplotypes
  • Humans
  • Immunoglobulins, Intravenous / therapeutic use
  • Lectins, C-Type / genetics*
  • Linkage Disequilibrium
  • Mucocutaneous Lymph Node Syndrome / diagnosis
  • Mucocutaneous Lymph Node Syndrome / genetics*
  • Mucocutaneous Lymph Node Syndrome / therapy
  • Polymorphism, Single Nucleotide
  • Receptors, Cell Surface / genetics*
  • Treatment Outcome

Substances

  • Cell Adhesion Molecules
  • DC-specific ICAM-3 grabbing nonintegrin
  • Immunoglobulins, Intravenous
  • Lectins, C-Type
  • Receptors, Cell Surface

Grants and funding

This work was supported by a grant from the National Science Council, Taiwan (NSC 102-2314-B-182-053-MY3), Taipei Medical University, Taiwan (Grant no. TMU101-AE1-B14) and grants from Chang Gung Memorial Hospital, Taiwan (CMRPG8C1081 and CMRPG8B0211). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.