The lack of immune response to an antigen, a process known as immune tolerance, is essential for the preservation of immune homeostasis. To date, two mechanisms that drive immune tolerance have been described extensiv...The lack of immune response to an antigen, a process known as immune tolerance, is essential for the preservation of immune homeostasis. To date, two mechanisms that drive immune tolerance have been described extensively： central tolerance and peripheral tolerance. Under the new nomenclature, thymus-derived regulatory T （tTreg） ceils are the major mediators of central immune tolerance, whereas peripherally derived regulatory T （PTreg） cells function to regulate peripheral immune tolerance. A third type of Treg ceils, termed iTreg, represents only the in vitro-induced Treg cellsz. Depending on whether the cells stably express Foxp3, pTreg, and iTreg cells may be divided into two subsets： the classical CD4＋Foxp3＋ Treg cells and the CD4＋Foxp3- type 1 regulatory T （Trl） cells2. This review focuses on the discovery, associated biomarkers, regulatory functions, methods of induction, association with disease, and clinical trials of Trl cells.展开更多
文摘The lack of immune response to an antigen, a process known as immune tolerance, is essential for the preservation of immune homeostasis. To date, two mechanisms that drive immune tolerance have been described extensively： central tolerance and peripheral tolerance. Under the new nomenclature, thymus-derived regulatory T （tTreg） ceils are the major mediators of central immune tolerance, whereas peripherally derived regulatory T （PTreg） cells function to regulate peripheral immune tolerance. A third type of Treg ceils, termed iTreg, represents only the in vitro-induced Treg cellsz. Depending on whether the cells stably express Foxp3, pTreg, and iTreg cells may be divided into two subsets： the classical CD4＋Foxp3＋ Treg cells and the CD4＋Foxp3- type 1 regulatory T （Trl） cells2. This review focuses on the discovery, associated biomarkers, regulatory functions, methods of induction, association with disease, and clinical trials of Trl cells.
