摘要
自噬是广泛存在于真核细胞中的一条胞内蛋白的降解途径,它主要对体内的长寿蛋白及一些细胞器进行降解。某些疾病的病理机制与细胞内蛋白的异常聚积并形成聚集体和包涵体有关,其分子机制与p62、LC3及其参与的细胞自噬异常有关。细胞自噬及其形成的自噬小体不仅与MHCⅡ类分子抗原提呈途径有关,而且与专职APC细胞对MHCI类分子的交叉提呈途径有关。
Autophagy is an intraeellular protein degradation system that is found ubiquitously in eukaryotie cells. It is responsible for the degradation of most long-lived proteins and some organelles. Current researches showed that the pathomechanisms of some diseases are related to the aberrant accumulation of intracellular proteins and the formation of aggregates and inclusions. The molecular mechanism is due to the abnormal cellular autophagy in which p62 and LC3 involve. The autophagy and autophagosome were recently found to be involved not only in the MHC class Ⅱ presentation of antigen, but also in the cross-presentation of MHC Ⅰ molecules mediated by professinal APCs.
出处
《国际免疫学杂志》
CAS
北大核心
2009年第3期180-183,共4页
International Journal of Immunology
基金
基金项目:国家自然科学基金资助项目(30771999)
江苏省自然科学基金资助项目(BK2008296)