LILRA6基因拷贝数变异与特应性皮炎易感性相关。
LILRA6 copy number variation correlates with susceptibility to atopic dermatitis.
作者信息
López-Álvarez M R, Jiang W, Jones D C, Jayaraman J, Johnson C, Cookson W O, Moffatt M F, Trowsdale J, Traherne J A
机构信息
Immunology Division, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK.
Cambridge Institute for Medical Research, University of Cambridge, Cambridge Biomedical Campus, Wellcome Trust/MRC Building, Hills Road, Cambridge, CB2 0XY, UK.
出版信息
Immunogenetics. 2016 Oct;68(9):743-7. doi: 10.1007/s00251-016-0924-z. Epub 2016 Jun 22.
Leukocyte immunoglobulin-like receptors (LILR) are expressed mostly on myelomonocytic cells where they are mediators of immunological tolerance. Two LILR genes, LILRA3 and LILRA6, exhibit marked copy number variation. We assessed the contribution of these genes to atopic dermatitis (AD) by analysing transmission in 378 AD families. The data indicated that copies of LILRA6 were over-transmitted to affected patients. They are consistent with a contribution of LILR genes to AD. They could affect the equilibrium between activating and inhibitory signals in the immune response.
白细胞免疫球蛋白样受体（LILR）主要在骨髓单核细胞上表达，是免疫耐受的介质。两个LILR基因，即LILRA3和LILRA6，表现出明显的拷贝数变异。我们通过分析378个特应性皮炎（AD）家族中的遗传传递情况，评估了这些基因对特应性皮炎的作用。数据表明，LILRA6的拷贝过度传递给了患病患者。这些结果与LILR基因对特应性皮炎的作用相符。它们可能影响免疫反应中激活信号和抑制信号之间的平衡。
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