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

DC-SIGN gene promoter variants and IVIG treatment response in Kawasaki disease.
复制标题

DOI:
10.1186/1546-0096-11-32
复制
发表时间:
2013-09-05
期刊:
Pediatric rheumatology online journal
影响因子:
--
通讯作者:
Shrestha S
Shrestha S
中科院分区:
其他
文献类型:
--
作者:
Portman MA;Wiener HW;Silva M;Shendre A;Shrestha S

文献摘要

参考文献

被引文献

相似文献

抑制FcγRIIB的遗传变异介导抗炎反应并影响IVIG难治性(IVIG- r)。然而,这些变异在亚洲和西班牙裔人群中很少见,因此该途径中的其他基因可能参与其中。IVIG在缺乏与人类DC-SIGN相关的分子SIGN-R1的小鼠中无效。此外,DC-SIGN是唾液化Fc的已知受体,该成分负责IVIG的抗炎作用。因此,我们假设DC-SIGN也可能参与川崎病(KD)患者IVIG应答通路。采用病例对照方法,研究了白人(158人对62人)、亚洲人(64人对12人)和西班牙人(55人对20人)KD患者中带有IVIG-R的DC-SIGN启动子中5个单核苷酸多态性(snp)的差异分布。在三个民族中,DC-SIGN启动子中几个变异的等位基因频率分布存在明显差异。此外,具有rs2287886主要等位基因“A”的亚洲人更有可能成为IVIG无应答者(OR = 1.76, p = 0.04),但该等位基因在其他两个种族中是一个次要等位基因,其相关性不明显。DC-SIGN可能在参与IVIG反应机制的抗炎级联中补充fc - γ riib的作用。
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. 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. DC-SIGN can potentially complement the role of FcγRIIB in the anti-inflammatory cascade involved in the IVIG response mechanism.
DOI: 10.1097/inf.0b013e3181cf8705
发表时间: 2010-06-01
影响因子: 3.6
作者:
Holman, Robert C.;Belay, Ermias D.;Schonberger, Lawrence B.
通讯作者: Schonberger, Lawrence B.
DOI: 10.1097/00006454-199812000-00009
发表时间: 1998-12-01
影响因子: 3.6
作者:
Burns, JC;Capparelli, EV;Glode, MP
通讯作者: Glode, MP
DOI: 10.1073/pnas.0810163105
发表时间: 2008-12-16
影响因子: 11.1
作者:
Anthony, Robert M.;Wermeling, Fredrik;Ravetch, Jeffrey V.
通讯作者: Ravetch, Jeffrey V.
DOI: 10.1128/jvi.78.24.14053-14056.2004
发表时间: 2004-12-01
影响因子: 5.4
作者:
Martin, MP;Lederman, MM;Carrington, M
通讯作者: Carrington, M
DOI: 10.1016/j.jcv.2008.06.005
发表时间: 2008-10-01
影响因子: 8.8
作者:
Chaudhary, Omkar;Rajsekar, Kavitha;Luthra, Kalpana
通讯作者: Luthra, Kalpana