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首页> 外文期刊>Neuron >Neuroprotection from Stroke in the Absence of MHCI or PirB
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Neuroprotection from Stroke in the Absence of MHCI or PirB

机译：缺乏MHCI或PirB对中风的神经保护作用

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Recovery from stroke engages mechanisms of neural plasticity. Here we examine a role for MHC class I (MHCI) H2-Kb and H2-Db, as well as PirB receptor. These molecules restrict synaptic plasticity and motor learning in the healthy brain. Stroke elevates neuronal expression not only of H2-Kb and H2-Db, but also of PirB and downstream signaling. KbDb knockout (KO) or PirB KO mice have smaller infarcts and enhanced motor recovery. KO hippocampal organotypic slices, which lack an intact peripheral immune response, have less cell death after in vitro ischemia. In PirB KO mice, corticospinal projections from the motor cortex are enhanced, and the reactive astrocytic response is dampened after MCAO. Thus, molecules that function in the immune system act not only to limit synaptic plasticity in healthy neurons, but also to exacerbate brain injury after ischemia. These results suggest therapies for stroke by targeting MHCI and PirB. Adelson et al. find that MHC class I (MHCI) H2-Kb and K2-Db and their receptor, PirB, contribute to damage and restrict recovery after stroke. Levels of these molecules increase dramatically after stroke and their removal causes enhanced recovery, suggesting new therapeutic avenues.
机译：从中风恢复参与神经可塑性机制。在这里，我们研究了MHC I类（MHCI）H2-Kb和H2-Db以及PirB受体的作用。这些分子限制了健康大脑中的突触可塑性和运动学习。中风不仅提高了H2-Kb和H2-Db的神经元表达，还提高了PirB和下游信号的表达。 KbDb基因敲除（KO）或PirB KO小鼠的梗死面积较小，运动恢复增强。缺乏完整的外周免疫反应的KO海马器官型切片，在体外缺血后具有更少的细胞死亡。在PirB KO小鼠中，MCAO后，运动皮层的皮质脊髓投射增强，反应性星形细胞反应减弱。因此，在免疫系统中起作用的分子不仅起到限制健康神经元突触可塑性的作用，而且还加剧缺血后的脑损伤。这些结果表明通过靶向MHCI和PirB可以治疗中风。 Adelson等。发现MHC I类（MHCI）H2-Kb和K2-Db及其受体PirB有助于损害并限制中风后的恢复。这些分子的水平在中风后急剧增加，其去除导致增强的恢复，提示了新的治疗途径。

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