树突状细胞、过表达细胞因子转导抑制因子1的树突状细胞及T细胞在慢性阻塞性肺疾病发病机制中的研究进展

Research advance of dendritic cells,suppressor of cytokine signaling-1 overexpressed dendritic cells and T lymphocytes in the pathogenesis of chronic obstructive pulmonary disease

越来越多的研究表明自身免疫反应参与了慢性阻塞性肺疾病(COPD)发病机制,暗示COPD的发病过程可能与免疫系统的调节紊乱有关。树突状细胞(DCs)及T细胞作为重要的免疫细胞,可能参与了COPD的免疫病理机制。细胞因子信号转导抑制因子1(SOCS1)作为一类JAK-STAT信号传导途径中重要的负性调节者,通过对JAKs的抑制,有助于负反馈调节多种细胞因子信号,影响细胞的分化及功能。因此,SOCS1通过修饰并调节DCs的功能可能在自身免疫性疾病中发挥重要作用。同时,过表达SOCS1能够修饰DCs,使其偏向于未成熟树突状细胞(im DCs),并维持其未成熟状态,诱导机体的免疫耐受,进而参与自身免疫性疾病。该文将对DCs、T细胞及过表达SOCS1的树突状细胞(DC-SOCS1)在COPD发病机制中的可能作用进行综合阐述。

A growing body of studies have identified that autoimmune may take part in the pathogenesis of chronic obstructive pulmonary disease（COPD）,which hints the pathogenesis of COPD maybe associated with the regulating disorder of immune system. Dendritic cells（DCs） and T lymphocytes as immportant immune cell maybe contribute to the immunopathology of COPD. Suppressor of cytokine signaling-1（SOCS1） is a key negative regulator of the JAK-STAT signal pathway and serves to negatively regulate signaling of various cytokines by inhibiting the Janus kinases（JAKs）,then affects the function and differentiation of cells. So,SOCS1 maybe play an essential role in autoimmunity through modifying and affecting the function of DCs. Simultaneously,overexpression SOSC1 can modify DCs,making it tend to be immune dendritic cells（im DCs） and maintaining its immaturity,then establish immune tolerance,which participates in autoimmune disease. Here,we will elaborate the possible contrbution of dendritic cells（DCs）,T lymphocytes and suppressor of cytokine signaling-1 overexpressed dendritic cells（DC-SOCS1） in pathogenesis of COPD.