Nik Tavakoli Nasim, Hambly Brett D, Sullivan David R, Bao Shisan
Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney, New South Wales 2006, Australia.
Int J Biochem Cell Biol. 2008;40(11):2369-73. doi: 10.1016/j.biocel.2007.10.004. Epub 2007 Oct 10.
CD4+CD25+ regulatory T (Treg) cells play a crucial role in maintaining self-tolerance and preventing autoimmune disease. The transcription factor forkhead box protein 3 (Foxp3) has been identified as a molecular marker for Treg cells. Foxp3 is highly expressed in lymphoid tissue and several signalling pathways influence its expression. It plays an essential role in the development and function of Treg cells. Mutations in Foxp3 are responsible for the scurfy (sf) mutant mouse, and for autoimmune human diseases including the X-linked fatal "immune dysregulation, polyendocrinopathy, enteropathy, X-linked" (IPEX), autoimmune colitis and rheumatoid arthritis. Recent studies have also revealed an important and novel anti-atherogenic role for Treg cells and consequently for Foxp3. These data open up potential novel therapeutic avenues for the management of atherosclerosis.
CD4+CD25+调节性T(Treg)细胞在维持自身耐受性和预防自身免疫性疾病中起关键作用。转录因子叉头框蛋白3(Foxp3)已被确定为Treg细胞的分子标志物。Foxp3在淋巴组织中高表达,并且有几种信号通路影响其表达。它在Treg细胞的发育和功能中起重要作用。Foxp3的突变导致了“头皮屑”(sf)突变小鼠以及包括X连锁致命性“免疫失调、多内分泌病、肠病、X连锁”(IPEX)、自身免疫性结肠炎和类风湿性关节炎在内的人类自身免疫性疾病。最近的研究还揭示了Treg细胞以及因此Foxp3在抗动脉粥样硬化方面的重要且新颖的作用。这些数据为动脉粥样硬化的治疗开辟了潜在的新途径。