角质形成细胞的异常增殖和炎症反应是银屑病特征性的病理改变。研究发现银屑病皮损处自噬受体P62表达明显升高，而内源性大麻素系统（ECS）的激活可以调节TLR4的表达，并进一步调控P62最终影响角质形成细胞自噬。基于上述基础，我们提出ECS通过CBR-TLR4-P62途径，影响角质细胞的自噬，降低银屑病角质形成细胞的增殖和炎症反应，从而发挥对银屑病治疗作用的科学假说。因此本课题拟通过研究临床患者内源性大麻素水平升高、P62基因表达与银屑病之间的关系，在动物和细胞水平探讨TLR4、P62的表达与角质形成细胞自噬激活之间的关系，并深入研究相关作用机制，为银屑病的临床干预和治疗提供新的思路。

The abnormal proliferation of keratinocyte and inflammation are characteristic changes of psoriasis. It is reported that the activation of endocannabinoids system (ECS) could regulate the expression of TLR4, which may affect the keratinocyte autophagy by controlling P62. We propose that ECS can affect the keratinocyte autophagy, reduce the proliferation of keratinocyte and inflammation in psoriasis through CBR-TLR4-P62 pathway，and therefore provide a potential therapy for psoriasis. In this project, we aim to explore the relationship between ECS activation, expression of P62 gene and psoriasis, discuss the relationship between the expression of TLR4, the expression of P62 and keratinocyte autophagy at the animal and cell molecular level, investigate the relevant mechanism further and provide new ideas as well as strategies for clinical intervention in psoriasis.