Radziewicz Henry, Dunham Richard M, Grakoui Arash
Emory Vaccine Center, Department of Microbiology and Immunology, Emory University School of Medicine, 954 Gatewood Road NE, Atlanta, GA 30329, USA.
J Clin Invest. 2009 Mar;119(3):450-3. doi: 10.1172/jci38661.
Adaptive T cell responses are critical for controlling infections with viruses such as HIV, HBV, and HCV. However, these responses must be carefully regulated because overly vigorous T cell activation can lead to excessive host tissue damage. T cell expression of the inhibitory receptor programmed death-1 (PD-1) and inhibition of effector T cells (Teffs) by CD4+Foxp3+Tregs are among the many described mechanisms for achieving a balanced immune response. Although the signals that contribute to Teff function are well understood, less is known about the signals controlling Tregs. In this issue of the JCI, Franceschini et al. extend our understanding of how Tregs are modulated during chronic HCV infection by demonstrating that Treg proliferation is inhibited by PD-1 and that this inhibition is mediated by a potentially novel mechanism involving the prevention of IL-2-driven STAT-5phosphorylation.
适应性T细胞反应对于控制诸如HIV、HBV和HCV等病毒感染至关重要。然而，这些反应必须得到严格调控，因为过度活跃的T细胞激活会导致宿主组织过度损伤。抑制性受体程序性死亡-1（PD-1）在T细胞上的表达以及CD4+Foxp3+调节性T细胞（Tregs）对效应T细胞（Teffs）的抑制作用，是众多已被描述的实现平衡免疫反应的机制之一。尽管促成Teff功能的信号已为人熟知，但关于控制Tregs的信号却了解较少。在本期《临床研究杂志》中，弗朗切斯奇尼等人通过证明PD-1抑制Treg增殖，且这种抑制作用是由一种可能涉及阻止IL-2驱动的STAT-5磷酸化的新机制介导的，扩展了我们对慢性HCV感染期间Tregs如何被调节的理解。
