Mantegazza Adriana R, Marks Michael S
Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Cell Metab. 2016 Jul 12;24(1):11-2. doi: 10.1016/j.cmet.2016.06.022.
Mitochondrial dysfunction and T cell autoimmunity have been independently implicated in Parkinson disease pathogenesis. In a recent publication in Cell, Matheoud et al. (2016) link them by describing a new mechanism, activated in familial forms of Parkinson disease, in which mitochondrial proteins are processed for recognition by CD8+ T cells.
线粒体功能障碍和T细胞自身免疫已分别被认为与帕金森病的发病机制有关。在最近发表于《细胞》杂志的一篇文章中，马泰乌德等人（2016年）通过描述一种在帕金森病家族形式中被激活的新机制，将它们联系起来，在这种机制中，线粒体蛋白经过加工后被CD8+T细胞识别。
