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骨髓增生异常综合征T淋巴细胞异常与克隆造血
  • 期刊名称:白血病与淋巴瘤
  • 时间:0
  • 页码:71-75
  • 分类:R563.1[医药卫生—呼吸系统;医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:[1]中国中医科学院西苑医院血液科,北京100091
  • 相关基金:国家自然科学基金(30973903,30973812)
  • 相关项目:中药复方青黄散(青黛-雄黄)治疗骨髓增生异常综合征的克隆选择性与砷的体内效应相关性研究
作者: 胡晓梅|
中文摘要:

目的 了解T淋巴细胞异常在骨髓增生异常综合征(MDS)克隆造血中的作用。方法对76例MDS患者的染色体核型、T淋巴细胞亚群及激活状态进行分析。结果正常核型36例,异常核型40例,异常发生率52.6%。40例异常核型中,三体8(+8)24例,占异常核型的60.0%。与健康对照组比较,MDS患者CD;CD-19、CD+3;CD+3;CD+8;以及CD+3HLA—DR^+细胞百分率显著升高,CD-3(CD16CD56)^+细胞的百分率明显降低。将MDS患者进行核型分组,异常核型组CD+3(CD16CD56)^+细胞的百分率显著高于正常对照组。将+8核型从MDS异常核型中独立出来进行分析,CD+3CD+4CD-8细胞的百分率明显低于正常核型以及其他异常组,CD4/CD8的比值明显低于健康对照组。结论MDS存在T淋巴细胞异常,异常核型MDS可能恶性克隆增殖更为优势,预后更差。+8核型MDS存在更为严重的免疫监视功能下降,导致恶性克隆过度增殖与残存造血过度受抑。

英文摘要:

Objective To investigate the effect of dysfunction of T lymphocytes on clonal haematogenesis in patients with myelodysplastic syndrome (MDS). Methods The cytogentics, the subsets of lymphocytes and their activation in 76 patients with MDS were analyzed. Results There were 36 patients with normal karyotype and 40 patients with abnormal karyotype. The incidence of abnormal karyotype were 52.6 %. There were 24 cases (60.0 %) with trisomy 8 (+8) in 40 cases of abnormal karyotype. The expression rates of CD+3 CD-19 cells, CD+3 CD-4 CD+8 cells and CD+3 HLA-DR^+ cells in MDS were significantly increased, and CD-3 (CD16CD56)^+ cells were significantly lower than that in control group. The expression rates of CD; (CD16CD56)^+ cells in MDS with abnormal karyotype were significantly higher than that in control group. The expression rates of CD+3 CD+4 CD-8 cells in +8 MDS were significantly lower than that in MDS patients with normal karyotype and with other abnormal karyotype. The ratio of CD4/CD8 in +8 MDS were significantly lower than that in control group. Conclusion The abnormalities of T cell subsets and functions in patients with MDS were observed and the proliferation of malignant clone was prevalent which indicated a poor prognosis in MDS with abnormal karyotype. Dysfunction of immunosurveillance was more aggravated in +8 MDS, which led to excess proliferation of malignant clone and over inhibition of remaining haematogenesis.

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