T regulatory cells: hypoxia-adenosinergic suppression and re-direction of the immune response.
T regulatory cells: hypoxia-adenosinergic suppression and re-direction of the immune response.
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DOI：
10.1016/j.it.2008.12.002
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发表时间：
2009-03
影响因子：
16.8
通讯作者：
M. Sitkovsky
中科院分区：
文献类型：
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作者：
M. Sitkovsky
T 调节细胞（Treg 细胞）抑制免疫反应以维持自身耐受性，但它们也可以保护癌组织。我提出了一个模型来潜在地统一 Treg 细胞的不同功能。这假设 Treg 细胞为生理组织保护机制提供了一个互补的免疫臂，由发炎或癌组织中的低氧张力（即缺氧）驱动。 Treg 和效应细胞中 cAMP 升高的 A2A 和 A2B 腺苷受体、缺氧诱导转录因子 1α (HIF)、cAMP 反应元件 (CRE) 和缺氧反应元件 (HRE) 介导的转录在此模型中发挥关键作用。 Treg 细胞的 T 细胞受体 (TCR) 触发以及 HRE 和 CRE 驱动的活动都是实现最大水平的免疫抑制所必需的。
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 1α (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.