Targeting CD4+CD25+FoxP3+ regulatory T-cells for the augmentation of cancer immunotherapy.

Targeting CD4+CD25+FoxP3+ regulatory T-cells for the augmentation of cancer immunotherapy.
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发表时间:
2007-12
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通讯作者:
Rich-Henry Schabowsky;Shravan Madireddi;Rajesh Sharma;E. Yolcu;H. Shirwan
Rich-Henry Schabowsky;Shravan Madireddi;Rajesh Sharma;E. Yolcu;H. Shirwan
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作者:
Rich-Henry Schabowsky;Shravan Madireddi;Rajesh Sharma;E. Yolcu;H. Shirwan

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CD4+CD25+FoxP3+T细胞是维持外周自身免疫耐受的重要细胞,与外源性抗原耐受有关。越来越多的证据表明,Treg细胞也可能在癌症的免疫逃避机制中发挥重要作用。Treg细胞被肿瘤主动招募和诱导,阻断先天和获得性免疫启动、效应器功能和记忆反应,从而抑制治疗性肿瘤疫苗的疗效。因此,已经使用各种方法研究了Treg细胞在癌症中的功能调节,得到了令人鼓舞的临床前和临床结果。然而,控制和有效地调节Treg细胞的功能用于癌症治疗将取决于对Treg细胞与肿瘤细胞相互作用的分子基础以及随后的免疫抑制机制的更好理解。
CD4+CD25+FoxP3+ T-regulatory (Treg) cells are vital to the maintenance of peripheral self tolerance and are implicated in tolerance to foreign antigens. Increasing evidence shows that Treg cells may also play an important role in immune evasion mechanisms employed by cancer. Treg cells are actively recruited and induced by tumors to block innate and adaptive immune priming, effector function and memory response, which can inhibit the efficacy of therapeutic cancer vaccines. As such, modulation of Treg cell function in cancer has been studied using various approaches, with encouraging preclinical and clinical findings. However, controlled and effective modulation of Treg cell function for cancer therapeutics will be contingent on a better understanding of the molecular basis of Treg cell interaction with tumor cells and ensuing immunosuppressive mechanisms.