Department of Microbiology and Immunology, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
J Leukoc Biol. 2010 Jun;87(6):1011-8. doi: 10.1189/jlb.1209772. Epub 2010 Mar 24.
During the development of immune responses to pathogens, self-antigens, or environmental allergens, naive CD4(+) T cells differentiate into subsets of effector cells including Th1, Th2, and Th17 cells. The differentiation into these subsets is controlled by specific transcription factors. The activity of these effector cells is limited by nTregs and iTregs, whose differentiation and maintenance are dependent on the transcription factor Foxp3. The regulation of autoimmune diseases mediated by Th1 and Th17 cells by Tregs has been studied and reviewed extensively. However, much less has been presented about the interplay between Tregs and Th2 cells and their contribution to allergic disease. In this perspective, we discuss the regulation of Th2 cells by Tregs and vice versa, focusing on the interplay between the IL-4-activated STAT6/GATA3 pathway and Foxp3.
在对病原体、自身抗原或环境过敏原产生免疫反应的过程中，幼稚 CD4(+) T 细胞分化为效应细胞亚群，包括 Th1、Th2 和 Th17 细胞。这种亚群分化由特定的转录因子控制。这些效应细胞的活性受到 nTregs 和 iTregs 的限制，其分化和维持依赖于转录因子 Foxp3。Tregs 对 Th1 和 Th17 细胞介导的自身免疫性疾病的调节已经被广泛研究和综述。然而，关于 Tregs 和 Th2 细胞之间的相互作用及其对过敏疾病的贡献，人们知之甚少。在这篇观点文章中，我们讨论了 Tregs 对 Th2 细胞的调节作用以及反之亦然，重点讨论了 IL-4 激活的 STAT6/GATA3 途径与 Foxp3 之间的相互作用。
