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- Title
DC-SIGN gene promoter variants and IVIG treatment response in Kawasaki disease.
- Authors
Portman, Michael A.; Wiener, Howard W.; Silva, Miriam; Shendre, Aditi; Shrestha, Sadeep
- Abstract
Background: Genetic variants in the inhibiting FcаRIIB 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 FcаRIIB in the anti-inflammatory cascade involved in the IVIG response mechanism.
- Subjects
HUMAN genetic variation; LABORATORY mice; DENDRITIC cells; CELL adhesion molecules; MUCOCUTANEOUS lymph node syndrome; CORONARY disease; SINGLE nucleotide polymorphisms; PATIENTS
- Publication
Pediatric Rheumatology, 2013, Vol 11, Issue 1, p1
- ISSN
1546-0096
- Publication type
Article
- DOI
10.1186/1546-0096-11-32