KIR2DL4（CD158d）基因多态性与多发性硬化症易感性
KIR2DL4 (CD158d) polymorphisms and susceptibility to multiple sclerosis.
作者信息
Goris An, Dobosi Rita, Boonen Steven, Nagels Guy, Dubois Bénédicte
机构信息
Katholieke Universiteit Leuven, Belgium.
出版信息
J Neuroimmunol. 2009 May 29;210(1-2):113-5. doi: 10.1016/j.jneuroim.2009.03.001.
Several lines of evidence implicate CD56(bright) NK cells in the pathogenesis of multiple sclerosis (MS). This proposed immunoregulatory pathway involves already established susceptibility genes such as interleukin-2 receptor alpha (IL2RA) and interleukin-7 receptor (IL7R). We therefore investigated the CD56(bright) NK cell effector molecule KIR2DL4 for its involvement in genetic susceptibility to MS in a study population of 763 cases and 967 controls. Whereas 26% of the study population has a genotype corresponding to a lack of any functional membrane-bound form of the molecule, no association of the KIR2DL4 transmembrane alleles with susceptibility to MS was observed.
多条证据表明CD56（明亮型）自然杀伤细胞（NK细胞）参与了多发性硬化症（MS）的发病机制。这一提出的免疫调节途径涉及已确定的易感基因，如白细胞介素-2受体α（IL2RA）和白细胞介素-7受体（IL7R）。因此，我们在一个由763例病例和967例对照组成的研究群体中，研究了CD56（明亮型）NK细胞效应分子KIR2DL4与MS遗传易感性的关系。虽然26%的研究群体具有对应于缺乏该分子任何功能性膜结合形式的基因型，但未观察到KIR2DL4跨膜等位基因与MS易感性之间存在关联。
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