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目的探讨外周血白细胞CD11c/CD18表达与急性缺血性脑卒中(acute ischemic stroke,AIS)发病的关系。方法采用流式细胞术和单克隆抗体标记测定28例AIS患者(AIS组)发病72h内及病程第7d2次外周血中性粒细胞(PMN)和单核细胞(MNL)表面CD11c、CD18的表达量,以平均荧光强度(MFI)表示其相对含量,并与28名健康对照者(对照组)比较。结果AIS组发病72h内外周血PMN表面CD11c、CD18MFI分别为20.82±5.88、218.25±89.00;病程7d时为18.60±5.52、185.52±68.44;均显著高于对照组CD11c、CD18MFI(15.63±3.01、150.76±41.20);发病72h内外周血MNL表面CD11c、CD18MFI分别为34.78±14.56、286.75±95.50,病程7d时为31.97±14.47、247.00±88.06,均显著高于对照组CD11c、CD18MFI(20.20±8.50和186.38±52.97)(P<0.05~0.01);发病7d时CD11c、CD18MFI虽有所下降,但与发病72h内比较差异无显著性(P>0.05)。结论AIS时激活的PMN、MNL表面β2整合素CD11c、CD18表达上调,CD11c、CD18可能参与了炎症反应。
Objective To investigate the relationship between the expression of CD11c / CD18 in peripheral blood leukocytes and the pathogenesis of acute ischemic stroke (AIS). Methods The expressions of CD11c and CD18 on peripheral blood neutrophil (PMN) and mononuclear cells (MNL) in 28 patients with AIS (AIS group) within 72 hours and on the 7th day of disease course were determined by flow cytometry and monoclonal antibody. Amount, expressed as the relative fluorescence intensity (MFI), and compared with 28 healthy controls (control group). Results The CD11c and CD18MFI of PMN on the peripheral blood of AIS group were respectively 20.82 ± 5.88 and 218.25 ± 89.00 within 72 hours after onset of disease, and 18.60 ± 5.52 and 185.52 ± 68.44 on the 7th day of the AIS group. The CD11c and CD18MFI were significantly higher in the AIS group than those in the control group (15.63 ± 3.01,150.76 ± 41.20). The levels of CD11c and CD18MFI on peripheral blood MNL were 34.78 ± 14.56 and 286.75 ± 95.50 respectively in the 72h after onset and 31.97 ± 14.47 and 247.00 ± 88.06 on the 7th day after the onset of disease, both of which were significantly higher than those of the control group (CD11c, CD18MFI, 20.20 ± 8.50 and 186.38 ± 52.97) (P <0.05-0.01). Although CD11c and CD18MFI decreased on the 7th day, there was no significant difference between the two groups (P> 0.05). Conclusions The activation of PMN on AIS and the expression of β2 integrin CD11c and CD18 on MNL surface are upregulated. CD11c and CD18 may be involved in the inflammatory response.