Multiple sclerosis associates with LILRA3 deletion in Spanish patients

被引：0
|
作者：
D Ordóñez
A J Sánchez
J E Martínez-Rodríguez
E Cisneros
E Ramil
N Romo
M Moraru
E Munteis
M López-Botet
J Roquer
A García-Merino
C Vilches
机构：
[1] Inmunogenética - HLA,
[2] Hospital Universitario Puerta de Hierro,undefined
[3] Neuroinmunología,undefined
[4] Hospital Universitario Puerta de Hierro,undefined
[5] Neurología,undefined
[6] Hospital del Mar-Institut Municipal d′Investigació Mèdica (IMIM),undefined
[7] Molecular Immunopathology Unit,undefined
[8] IMIM-Hospital del Mar,undefined
[9] Universitat Pompeu Fabra,undefined
来源：
Genes & Immunity | 2009年 / 10卷
关键词：
chromosome 19; gene deletion; killer-cell Immunoglobulin-like receptors; leukocyte immunoglobulin-like receptors; multiple sclerosis; susceptibility;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
The genetic susceptibility to multiple sclerosis (MS) is only partially explained, and it shows geographic variations. We analyse here two series of Spanish patients and healthy controls and show that relapsing MS (R-MS) is associated with a gene deletion affecting the hypothetically soluble leukocyte immunoglobulin (Ig)-like receptor A3 (LILRA3, 19q13.4), in agreement with an earlier finding in German patients. Our study points to a gene-dose-dependent, protective role for LILRA3, the deletion of which synergizes with HLA-DRB1*1501 to increase the risk of R-MS. We also investigated whether the risk of suffering R-MS might be influenced by the genotypic diversity of killer-cell Ig-like receptors (KIRs), located only ∼400 kb telomeric to LILRA3, and implicated in autoimmunity and defence against viruses. The relationship of LILRA3 deletion with R-MS is not secondary to linkage disequilibrium with a KIR gene, but we cannot exclude some contributions of KIR to the genetic susceptibility to R-MS.
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页码：579 / 585
页数：6
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