CD8 ＋ T淋巴细胞在急性脑梗死后肺炎发病中的作用

目的采用实验室检测结合临床评估手段，探索CD8^＋ T淋巴细胞在急性脑梗死后肺炎发病中的作用。 方法收集2014年12至2016年12月在同济大学附属上海东方医院神经内科和东南大学医学院附属江阴市人民医院神经内科住院治疗的急性脑梗死患者60例为研究对象。在脑梗死发病48 h内收集患者静脉血，分离外周血单核细胞，检测细胞表面CD107a，细胞内干扰素γ（IFN-γ）和肿瘤坏死因子α（TNF-α）。依据入组后住院期间是否发生肺炎将60例病例分为发生肺炎组和未发生肺炎组，采用t检验比较肺炎组混合病毒多肽干预及未干预患者、未发生肺炎组混合病毒多肽干预及未干预患者四者之间的外周血单核细胞层细胞表面CD107a脱颗粒、细胞内IFN-γ和TNF-α表达的差异。 结果在混合病毒多肽刺激CD8^＋ T淋巴细胞后，肺炎组细胞表面CD107a^＋表达低于未发生肺炎组［（10.6±3.7）% vs （15.6±4.3）%）］，细胞内IFN-γ^＋表达低于非肺炎组［（15.3±4.3）% vs （20.0±5.1）%］，TNF-α^＋表达低于未发生肺炎组［（15.1±4.4）% vs （19.3±4.7）%］，差异均具有统计学意义（t=3.192，P=0.004；t=4.127，P<0.001；t=3.621，P<0.001）；在未经混合病毒多肽刺激时，肺炎组细胞内IFN-γ^＋表达低于非肺炎组［（3.0±1.2）% vs （3.6±1.7）%）］，TNF-α^＋表达低于未发生肺炎组［（3.3±1.4）% vs （4.1±2.1）%］，差异也具有统计学意义（t=3.734，P<0.001；t=3.189，P=0.004）。 结论CD8^＋ T淋巴细胞的细胞毒性作用抑制可能是急性脑梗死患者发生肺炎的重要机制之一。

Role of CD8 + T lymphocytes in pathogenesis of pneumonia after acute cerebral infarction

ObjectiveTo explore the role of CD8⁺ T lymphocyte in the pathogenesis of pneumonia after acute cerebral infarction by laboratory testing combined with clinical evaluation. MethodsA total of 60 patients with acute cerebral infarction hospitalized at Department of Neurology of East Hospital Affiliated to Tongji University and Jiangyin People′s Hospital Affiliated to Southeast University from December 2014 to December 2016 were enrolled. Venous blood was collected from patients with cerebral infarction in 48 h of onset, and peripheral blood mononuclear cells were isolated. Cellular CD107a, intracellular IFN-γ and TNF-α were detected. According to whether pneumonia occurred during hospitalization, the 60 cases were divided into a pneumonia group or a non-pneumonia group. The difference in the positive expression of CD107a, IFN-γ and TNF-α was compared among the pneumonia group stimulated with hybrid viral peptides, non-pneumonia group stimulated with hybrid viral peptides, pneumonia group without hybrid viral peptide stimulation and non-pneumonia group without hybrid viral peptide stimulation. ResultsAfter stimulation with the hybrid viral peptides, CD107a positive expression rates in CD8⁺ T lymphocytes (10.6±3.7% vs 15.6±4.3%, t=3.192, P=0.004) and intracellular IFN-γ (15.3±4.3)% vs (20.0±5.1)%, t=4.127, P<0.001] and TNF-α positive expression rates (15.1±4.4)% vs (19.3±4.7)%, t=3.621, P<0.001] were significantly lower in the pneumonia group than in the non-pneumonia group. Without stimulation with the hybrid viral peptides, intracellular IFN-γ (3.0±1.2)% vs (3.6±1.7)%, t=3.734, P<0.001] and TNF-α positive expression rates (3.3±1.4)% vs (4.1±2.1)%, t=3.189, P=0.004] were significantly lower in the pneumonia group than in the non-pneumonia group. ConclusionThe inhibition of cytotoxicity of CD8⁺ T lymphocytes is an important mechanism involved in the pathogenesis of pneumonia after acute cerebral infarction.