研究显示子宫内膜异位症患者盆腹腔局部免疫微环境异常，免疫细胞不仅不能清除异位子宫内膜，反而促进其种植生长。我们近期发现，内异症患者腹腔液中CD56+CD16-NK细胞比例增加，异位病灶子宫内膜间质细胞（ESC）自噬水平降低，同时与CD16作用相关的造血细胞激酶（Hck）在低自噬ESC中也显著下降。将低自噬ESC与外周NK细胞体外共培养可以促进CD56+CD16-NK细胞分化。然而低自噬ESC是否通过Hck诱导CD56+CD16-NK细胞分化，耐受型NK细胞在内异症发病中发挥什么作用，这些均不清楚。本课题构建体外共培养体系和内异症小鼠模型，拟解析低自噬水平ESC通过Hck介导CD56+CD16-NK细胞分化的分子机制，进一步探讨CD56+CD16-NK细胞调控子宫内膜生长和侵袭参与EMs发病的分子机制。本课题将为内异症发病机制的研究提供新的研究方向，为寻找内异症的防治新策略提供科学依据。

There is strong evidence to support the role of abnormal immune response of peritoneal environment in endometriosis. Instead of leading to the clearance of regurgitated endometrial cells in pelvic cavity, dysregulated immune cells from endometriotic milieu are thought to favor the implantation and growth of ectopic endometrial tissue. Recently, we have found that the ratio of CD56+CD16- NK cells in peritoneal fluid is increased in endometriosis (stage III-IV), and the autophagy level is significantly lower in endometriosis-derived endometrial stromal cells (ESCs), as well as the expression of CD16-related hematopoietic cellular kinase (Hck). And ectopic ESCs could induce the CD56+CD16- NK cells differentiation in vitro. However, the mechanism behind the CD56+CD16- NK cell differentiation and its role in the progression of endometriosis is still unknown. Therefore, the aim of this study is to investigate how ESC autophagy in the endometriotic milieu regulates the CD56+CD16- NK cells differentiation through Hck and its downstream cytokines, and how these educated NK cells effect on the initiation and progression of endometriosis in vivo and in vitro. These findings have implications for future therapeutic strategies specifically targeting the abnormal autophagy in endometriosis.