DC-SIGN gene promoter variants and IVIG treatment response in Kawasaki disease

Background: genetic 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.findings: a 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.conclusions: dc-sign can potentially complement the role of fcγriib in the anti-inflammatory cascade involved in the ivig response mechanism. © 2013 portman et al.; licensee biomed central ltd.