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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >Factors regulating apoptosis and homeostasis of CD4+ CD25(high) FOXP3+ regulatory T cells are new therapeutic targets.
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Factors regulating apoptosis and homeostasis of CD4+ CD25(high) FOXP3+ regulatory T cells are new therapeutic targets.

机译:调节CD4 + CD25(高)FOXP3 +调节性T细胞凋亡和稳态的因素是新的治疗靶点。

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CD4+ CD25(high) Foxp3+ regulatory T cells (Tregs), as an active mechanism of immune suppression, have been targeted due to their tremendous therapeutic potentials to prevent autoimmune diseases, transplant rejection, and to inhibit progression of tumors and chronic viral diseases. In last twelve years, substantial molecular differences between homeostasis of Tregs and that of other subsets of T cells and some factors specific in regulation of Treg survival have been characterized. In this overview we focus on panoramic reviewing of 91 factors, pathways and drugs, both well-characterized and newly defined, regarding the survival and homeostasis of Tregs in the following sections: 2: Tregs, an essential mechanism of immune tolerance; 3: nTregs, aTregs and other regulatory T cells; 4: co-stimulation receptor signaling; 5: innate immunity and Toll-like receptor (TLR) signaling; 6: effects of cytokines and hormones; 7: transcription factors in regulation of Tregs; 8: Treg intracellular signaling pathways; 9: drugs and potential therapeutics; and 10: Treg cell survival and death. We recently reported that removal of Tregs via a Bax-dependent apoptotic pathway significantly enhances anti-self antigen immune responses, which demonstrated for the first time the proof of principle that apoptosis of Tregs is a new therapeutic target. Therefore, continued characterization of Treg apoptosis and homeostasis pathways would further improve our understanding in regulation of immune responses by cytokines, hormones and drugs, and would also lead to development of new therapeutics.
机译:CD4 + CD25(高)Foxp3 +调节性T细胞(Tregs)作为免疫抑制的一种主动机制,由于其具有巨大的治疗潜力,可预防自身免疫性疾病,移植排斥以及抑制肿瘤和慢性病毒性疾病的发展,因此已成为靶向治疗。在最近的十二年中,已经表征了Treg与其他T细胞亚群的稳态之间的实质性分子差异以及调节Treg存活的某些特异性因子。在本概述中,我们重点介绍以下几节中有关Treg的存活率和体内稳态的91种因素,途径和药物的概述,这些因素,途径和药物均已被很好地描述和重新定义:2:Treg,是免疫耐受的基本机制; 3:nTreg,aTreg和其他调节性T细胞; 4:共刺激受体信号;图5:先天免疫和Toll样受体(TLR)信号; 6:细胞因子和激素的作用; 7:调节Treg的转录因子;图8:Treg细胞内信号传导途径; 9:药物和潜在疗法10:Treg细胞存活和死亡。我们最近报道,通过Bax依赖性凋亡途径去除Tregs显着增强了抗自身抗原免疫反应,这首次证明了Tregs的凋亡是一种新的治疗靶点的原理证明。因此,对Treg细胞凋亡和动态平衡途径的持续表征将进一步增进我们对细胞因子,激素和药物对免疫反应的调节的了解,也将导致新疗法的发展。

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