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Decreased Expression of T-Cell Costimulatory Molecule CD28 on CD4 and CD8 T Cells of Mexican Patients with Pulmonary Tuberculosis

机译:T细胞共刺激分子CD28在墨西哥肺结核患者CD4和CD8 T细胞上的表达降低

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摘要

Patients with tuberculosis frequently develop anergy, a state of T-cell hyporesponsiveness in which defective T-cell costimulation could be a factor. To know if the expression of T-cell costimulatory molecules was altered in tuberculosis, we analyzed the peripheral blood T-cell phenotype of 23 Mexican patients with pulmonary tuberculosis. There was severe CD4 (P < .001) and CD8 (P < .01) lymphopenia and upregulation of costimulatory molecule CD30 on CD4 and CD8 T cells (P < .05); this increase was higher in relapsing tuberculosis. The main finding was severe downregulation of the major costimulatory molecule CD28 on both CD8 and CD4 T cells (P < .001). Depletion of the CD4/CD28 subset, a hitherto undescribed finding, is relevant because CD4 T cells constitute the main arm of the cell-mediated antimycobacterial immune response.
机译:肺结核患者经常出现无反应,这是T细胞反应低下的状态,其中不良的T细胞共刺激可能是一个因素。要了解结核病中T细胞共刺激分子的表达是否发生改变,我们分析了23名墨西哥肺结核患者的外周血T细胞表型。严重的CD4(P <.001)和CD8(P <.01)淋巴细胞减少和CD4和CD8 T细胞上共刺激分子CD30的上调(P <.05);复发性结核病的增加幅度更大。主要发现是CD8和CD4 T细胞上主要共刺激分子CD28的严重下调(P <0.001)。迄今为止尚未描述的CD4 / CD28子集的耗竭是相关的,因为CD4 T细胞构成了细胞介导的抗分枝杆菌免疫反应的主要部分。

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