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阿扎胞苷在体外和体内高风险骨髓增生异常综合征中差异影响 CD4(pos) T 细胞的极化。

Azacitidine differentially affects CD4(pos) T-cell polarization in vitro and in vivo in high risk myelodysplastic syndromes.

机构信息

Department of Hematology, VU University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands.

出版信息

Leuk Res. 2012 Jul;36(7):921-30. doi: 10.1016/j.leukres.2012.03.026. Epub 2012 Apr 14.

Abstract

CD4(pos) T-cell subsets play a role in myelodysplastic syndromes (MDS) pathogenesis and may be affected upon 5-azacitidine (Aza) treatment. Aza enhanced human T(H)1 frequencies in vitro but not in vivo. The proportion of functional FoxP3(pos) regulatory T cells (Treg) was enhanced by Aza in vitro (p < 0.0002), and a modest, temporary increase was observed in vivo (p = 0.08). The overall number of T(H)17 was reduced both in vitro (p < 0.03) and in vivo (p < 0.006), indicating that Aza directly affects CD4(pos) polarization during activation in vitro. Upon in vivo treatment in high risk MDS patients, particularly the T(H)17-Treg axis is affected.

摘要

CD4(pos) T 细胞亚群在骨髓增生异常综合征 (MDS) 的发病机制中起作用,并可能受到 5-氮杂胞苷 (Aza) 治疗的影响。Aza 在体外增强了人类辅助性 T(H)1 细胞频率,但在体内没有。Aza 在体外增强了功能性 FoxP3(pos) 调节性 T 细胞 (Treg) 的比例(p<0.0002),并且在体内观察到适度的暂时增加(p=0.08)。体外(p<0.03)和体内(p<0.006)均减少了 T(H)17 的总数,表明 Aza 在体外激活过程中直接影响 CD4(pos) 的极化。在高危 MDS 患者的体内治疗中,特别是 T(H)17-Treg 轴受到影响。

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