In this issue of Neuron, Dawes et al. (2018) show that CASPR2 antibodies (Abs) isolated from patients bind specifically to primary afferent cell bodies and induce neuropathic pain in mice. Consequent decreased expression of Kv1 channels and their aberrant localization along myelinated axons explain the observed hyperexcitability and pain.

中文翻译：

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自身抗体受伤：患者衍生的CASPR2抗体的转移引起小鼠神经性疼痛。

在本期《神经元》中，Dawes等人。（2018）显示从患者分离的CASPR2抗体（Abs）与原发传入细胞体特异性结合，并在小鼠中诱发神经性疼痛。随之而来的是Kv1通道的表达减少以及它们沿髓鞘轴突的异常定位，解释了观察到的过度兴奋和疼痛。