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通过流式细胞术对急性和慢性实验性过敏性肺炎进行支气管肺泡灌洗T细胞和Ia抗原定量分析。

Bronchoalveolar lavage T-cell and Ia antigen quantitation by flow cytometry in acute and chronic experimental hypersensitivity pneumonitis.

作者信息

Upadrashta B S, Adams P A, Kopp W C, Richerson H B

机构信息

Department of Internal Medicine, University of Iowa, Iowa City.

出版信息

Exp Lung Res. 1989 May;15(3):359-73. doi: 10.3109/01902148909087865.

Abstract

Increasing evidence implicates effector T-cells in the pathogenesis of hypersensitivity pneumonitis. We utilized T-cell- and Ia-specific antibodies, flow cytometry, and computer analysis to quantitate T-cell numbers and Ia expression on lung cells of established rabbit models of acute and chronic hypersensitivity pneumonitis (HSP). We used analysis of variance (ANOVA) and Turkey's follow-up to evaluate group differences. In the acute HSP group, increased percentages of T-cells and greater Ia expression were present on bronchoalveolar lavage (BAL) cells at 24 h after inhalational allergen challenge. Increased BAL T-cell numbers were found in the chronic HSP group produced by repeated inhalation of antigen and muramyl dipeptide, compared to "desensitized" animals and control groups. Both chronic HSP and desensitized groups demonstrated increased Ia expression on BAL cells. Pathology scores for individual animals in both acute and chronic protocols correlated significantly (Pearson correlation coefficients) with total numbers of BAL cells, percentages of T-cells, and percentages of Ia-positive cells recovered. Findings are consistent with the hypothesis that cell-mediated hypersensitivity is a central mechanism in the pathogenesis of experimental hypersensitivity pneumonitis.

摘要

越来越多的证据表明效应T细胞参与了过敏性肺炎的发病机制。我们利用T细胞和Ia特异性抗体、流式细胞术以及计算机分析,对急性和慢性过敏性肺炎(HSP)成熟兔模型的肺细胞中的T细胞数量和Ia表达进行定量分析。我们使用方差分析(ANOVA)和Turkey后续检验来评估组间差异。在急性HSP组中,吸入过敏原激发后24小时,支气管肺泡灌洗(BAL)细胞上T细胞百分比增加,Ia表达增强。与“脱敏”动物和对照组相比,通过反复吸入抗原和胞壁酰二肽产生的慢性HSP组中,BAL T细胞数量增加。慢性HSP组和脱敏组的BAL细胞上均显示Ia表达增加。急性和慢性实验方案中个体动物的病理评分与回收的BAL细胞总数、T细胞百分比以及Ia阳性细胞百分比显著相关(Pearson相关系数)。这些发现与细胞介导的超敏反应是实验性过敏性肺炎发病机制中的核心机制这一假说一致。

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