Intensive chemotherapy for acute myeloid leukemia differentially affects circulating TC1, TH1, TH17 and TREG cells.
Intensive chemotherapy for acute myeloid leukemia differentially affects circulating TC1, TH1, TH17 and TREG cells.
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DOI：
10.1186/1471-2172-11-38
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发表时间：
2010-07-09
期刊：
影响因子：
3
通讯作者：
Bruserud Ø
中科院分区：
文献类型：
--
作者：
Ersvaer E;Liseth K;Skavland J;Gjertsen BT;Bruserud Ø
一些观察表明，化疗后早期的免疫事件，可能是在严重的治疗引起的细胞减少时期，对于急性髓系白血病(AML)的抗白血病免疫反应是重要的。因此，我们研究了各种T细胞亚群(TC1、TH1、TH17)和CD25+FoxP3+Treg细胞在初治和强化化疗后的AML患者中的频率。严重化疗所致细胞减少的患者外周血中Tc1和TH1细胞的相对水平降低，而TH17的水平与健康对照组无差异。在未经治疗的AML患者中，在化疗引起的细胞减少和治疗后的再生过程中，CD25+FoxP3+T细胞的调节性水平升高。健康男性的Th17和TH1水平显著高于女性，但在化疗引起的细胞减少期间没有检测到这种性别差异。最后，外源性IL17-A通常对原代人AML细胞的增殖没有或仅有轻微影响。结论：急性髓系白血病强化化疗的疗效因循环T细胞亚群不同而异，TH17细胞相对频率不受化疗影响，这一亚群可能通过免疫调节作用间接影响AML细胞，但可能不是通过IL17-A的直接作用。
Several observations suggest that immunological events early after chemotherapy, possibly during the period of severe treatment-induced cytopenia, are important for antileukemic immune reactivity in acute myeloid leukemia (AML). We therefore investigated the frequencies of various T cell subsets (TC1, TH1, TH17) and CD25+ FoxP3+ TREG cells in AML patients with untreated disease and following intensive chemotherapy. Relative levels of circulating TC1 and TH1 cells were decreased in patients with severe chemotherapy-induced cytopenia, whereas TH17 levels did not differ from healthy controls. Increased levels of regulatory CD25+ FoxP3+ T cells were detected in AML patients with untreated disease, during chemotherapy-induced cytopenia and during regeneration after treatment. TH17 and TH1 levels were significantly higher in healthy males than females, but this gender difference was not detected during chemotherapy-induced cytopenia. Finally, exogenous IL17-A usually had no or only minor effects on proliferation of primary human AML cells. We conclude that the effect of intensive AML chemotherapy differ between circulating T cell subsets, relative frequencies of TH17 cells are not affected by chemotherapy and this subset may affect AML cells indirectly through their immunoregulatory effects but probably not through direct effects of IL17-A.