Department of Hematology, VU University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, The Netherlands.
Leuk Res. 2012 Jul;36(7):921-30. doi: 10.1016/j.leukres.2012.03.026. Epub 2012 Apr 14.
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.
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。