Analysis of autophagy deficiency-related disease by mouse model

我们使用自噬相关蛋白缺陷的突变小鼠研究了自噬在调节先天免疫反应中的作用。我们产生了Atg9a缺陷小鼠，发现Atg9a控制胚胎成纤维细胞中dsDNA诱导的先天免疫应答。由于dsDNA对先天免疫应答的异常激活通常导致大规模炎症的发展，因此Atg9a功能的调节可能有助于dsDNA诱导的炎性疾病的治疗。

We have examined a role of autophagy in the regulation of innate immune response using mutant mice deficient in autophagy-related protein. We generated Atg9a-deficient mice and found that Atg9a controls dsDNA-induced innate immune response in embryonic fibroblasts. Because aberrant activation of innate immune response by dsDNA often results in the development of massive inflammation, a regulation of Atg9a function might be useful for the therapy of inflammatory disease induced by dsDNA.