Sitkovsky Michail V
New England Inflammation and Tissue Protection Institute, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.
Trends Immunol. 2009 Mar;30(3):102-8. doi: 10.1016/j.it.2008.12.002. Epub 2009 Feb 7.
T regulatory cells (Treg cells) suppress immune responses to maintain self tolerance, but they also protect cancerous tissues. I propose a model to potentially unify the diverse functions of Treg cells. This assumes that Treg cells provide a complementary immunological arm to a physiological tissue-protecting mechanism, driven by low oxygen tension (i.e. hypoxia) in inflamed or cancerous tissues. The cAMP-elevating A2A and A2B adenosine receptors, hypoxia inducible transcription factor 1alpha (HIF), the cAMP response element (CRE)- and hypoxia response element (HRE)-mediated transcription in Treg and effector cells have key roles in this model. Both the T cell receptor (TCR)-triggered- and HRE- and CRE-driven activities of Treg cells are required to achieve a maximal level of immune suppression.
调节性T细胞（Treg细胞）抑制免疫反应以维持自身耐受性，但它们也会保护癌组织。我提出了一个模型，有可能统一Treg细胞的多种功能。该模型假设，Treg细胞为一种由炎症或癌组织中的低氧张力（即缺氧）驱动的生理性组织保护机制提供了一种互补的免疫分支。在该模型中，能提高环磷酸腺苷（cAMP）水平的A2A和A2B腺苷受体、缺氧诱导转录因子1α（HIF）、Treg细胞和效应细胞中由cAMP反应元件（CRE）和缺氧反应元件（HRE）介导的转录起着关键作用。Treg细胞的T细胞受体（TCR）触发活性以及HRE和CRE驱动的活性对于实现最大程度的免疫抑制都是必需的。
