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目的:研究Toll样受体7(Toll-like receptor 7,TLR7)mRNA及TLR9 mRNA在慢性粒细胞白血病(chronic myeloid leukemia,CML)患者外周血浆细胞样树突状细胞(plasmacytoid dendritic cell,pDC)内的表达及pDC分泌干扰素-α(interferon-α,IFN-α)的能力。方法:收集兰州大学第二医院血液科2010年11月至2011年7月间收治的30例CML患者(初诊未治组15例,缓解组15例)和体检中心的15例健康对照者,运用免疫磁珠法分选外周血pDC,利用real time-PCR检测pDC内TLR7及TLR9 mRNA表达水平。CpG ODN 2216刺激pDC 24 h后,ELISA检测上清液中IFN-α水平。结果:初诊组CML患者外周血pDC内TLR7 mRNA表达水平显著低于缓解组[(0.34±0.11)vs(0.93±0.21),P<0.05],初诊CML患者TLR9 mRNA表达水平显著低于缓解组[(0.44±0.15)vs(0.94±0.18),P<0.05]。CpG ODN 2216刺激后,初诊组pDC产生的IFN-α明显低于缓解组及健康对照组[(408.61±77.11)vs(611.39±84.86)、(651.67±93.39)ng/L,P<0.05]。结论:CML患者pDC内TLR7和TLR9 mRNA明显降低可能是pDC功能缺陷的主要原因,提示TLR7和TLR9可能参与CML的发病。
Objective: To investigate the expression of TLR7 mRNA and TLR9 mRNA in plasmacytoid dendritic cells (pDC) of patients with chronic myeloid leukemia (CML) And the ability of pDC to secrete interferon-α (IFN-α). Methods: Thirty CML patients (15 newly diagnosed group, 15 remission group) and 15 healthy control subjects were collected from Department of Hematology, Second Hospital of Lanzhou University from November 2010 to July 2011, Peripheral blood pDC was sorted by immunomagnetic beads method. The expression of TLR7 and TLR9 mRNA in pDC was detected by real time-PCR. After stimulation of pDC with CpG ODN 2216 for 24 h, the level of IFN-α in the supernatant was measured by ELISA. Results: The expression of TLR7 mRNA in the peripheral blood of newly diagnosed CML patients was significantly lower than that of the remission group [(0.34 ± 0.11) vs (0.93 ± 0.21), P <0.05], and the expression of TLR9 mRNA in newly diagnosed CML patients was significantly lower than that of the remission group [ (0.44 ± 0.15) vs (0.94 ± 0.18), P <0.05]. After CpG ODN 2216 stimulation, the IFN-α production of pDC in newly diagnosed group was significantly lower than that in remission group and healthy control group [(408.61 ± 77.11) vs (611.39 ± 84.86), (651.67 ± 93.39) ng / L, P <0.05]. Conclusion: The significant decrease of TLR7 and TLR9 mRNA in pDC may be the main reason of pDC dysfunction in CML patients, suggesting TLR7 and TLR9 may be involved in the pathogenesis of CML.