摘要
肠黏膜的免疫反应失控是炎症性肠病的特征性表现。机体的免疫和炎症系统被多种细胞因子调控,这些细胞因子如白细胞介素(IL)、干扰素等通过Janus激酶/信号转导和转录激活因子(JAK/STAT)途径发挥其生物功能。在炎症性肠病患者及小鼠结肠炎模型中均发现在STAT家族中以STAT3磷酸化程度最高,这提示STAT3的活化在炎症性肠病的发病中可能起着重要作用。此文就STAT3的功能、调节机制及其在炎症性肠病中可能发挥的作用的最新研究进行综述。
Inflammatory bowel disease (IBD) is characterized by a dysregulated mucosal immune response. Immune and inflammatory systems are controlled by multiple cytokines, including interleukins(IL) and interferons. These cytokines exert their biological functions through Janus tyrosine kinases and signal transducer and activators of transcription (JAK/STAT). Among STAT family members, STAT3 is the most strongly tyrosine phosphorylated in human IBD patients and the mice model of colitis, suggesting that STAT3 plays an important role in perpetuation of colitis. This review summarizes that the functional role of STAT3, negative feedback control of STAT3 activation and the role of STAT3 in IBD.
出处
《国际消化病杂志》
CAS
2007年第6期446-448,共3页
International Journal of Digestive Diseases
基金
云南省自然科学基金资助(编号2005C0069M)