摘要
Ⅰ型干扰素通路异常活化在系统性红斑狼疮(SLE)的发病机制中起着至关重要的作用。Ⅰ型干扰素可通过诱导外周血树突状细胞持续活化,直接作用或通过激活的树突状细胞诱导T、B细胞分化成熟,促进自身免疫反应;包含核酸的免疫复合物与FcγRⅡa、Toll受体结合是造成干扰素持续产生的重要因素;选择合适的靶点对干扰素通路进行干预有望成为SLE的一个有效的治疗手段;趋化因子积分和干扰素积分作为SLE新的生物标志物值得进一步的研究。
It plays a vital role that the type I interferon pathway is abnormally activated in the pathogenesis of SLE; The type I interferon can induce the sustained activation of peripheral blood dendritic cells,either directly or through the activation of dendritic cells induced by T-,B-cell differentiation and maturation,to promote their own immune response.It is the continuous production of interferon that is caused by the immune complexes of containing nucleic acids,FcγRIIa and Toll receptor.It is expected to be an effective treatment of SLE that the intervention of the interferon pathway through a suitable target.Chemokines and interferon integral deserve the further studies as the new biomarkers of SLE.
出处
《医学综述》
2010年第14期2109-2112,共4页
Medical Recapitulate
关键词
Ⅰ型干扰素
系统性红斑狼疮
趋化因子
The type Ⅰ interferon
Systemic lupus erythematosus
Chemokines
