Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90024, USA.
J Neuroimmunol. 2011 Mar;232(1-2):8-16. doi: 10.1016/j.jneuroim.2010.09.009. Epub 2010 Oct 14.
Mice deficient in classical major histocompatibility complex class I (MHCI) have aberrations in neurodevelopment. The consequences of upregulated neuronal MHCI expression have not been examined. We found that transgenic C57Bl/6 mice that are engineered to express higher levels of self-D(b) on their CNS neurons have alterations in their hippocampal morphology and retinogeniculate projections, as well as impaired neurorepair responses. Thus, enhanced neuronal classical MHCI expression can lead to aberrations in neural circuitry and neurorepair. These findings complement a growing body of knowledge concerning the neurobiological activities of MHCI and may have potential clinical relevance.
经典主要组织相容性复合体 I 类（MHCI）缺失的小鼠在神经发育方面存在异常。上调神经元 MHCI 表达的后果尚未得到检验。我们发现，经过基因工程改造在中枢神经系统神经元上表达更高水平自身 D(b)的 C57Bl/6 转基因小鼠，其海马形态和视网膜神经节投射发生改变，神经修复反应受损。因此，增强神经元经典 MHCI 表达可导致神经回路和神经修复异常。这些发现补充了越来越多的关于 MHCI 的神经生物学活性的知识，可能具有潜在的临床意义。
