Pertussis toxin treatment in vivo reduces surface expression of the adhesion integrin leukocyte function antigen-1 (LFA-1).

A R Schenkel, C D Pauza
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引用次数: 11

Abstract

Pertussis toxin treatment in macaques inhibits lymphocyte extravasation from the blood and leads to transient lymphocytosis and leukocytosis. We examined lymphocyte adhesion molecules known to be involved in the extravasation process to find possible mechanisms for the effects of pertussis toxin treatment. The two subunits of LFA-1, CD11a and CD18, showed decreased surface expression on lymphocytes from pertussis toxin treated animals compared to untreated animals. The adhesion molecule CD44, and the alpha subunit of the integrin VLA-4 (CD49d) were not decreased by pertussis toxin treatment. Lower surface expression of CD11a and CD18 was observed on all lymphocyte subsets and was correlated inversely with the extent of lymphocytosis. The magnitude of lymphocytosis after pertussis toxin treatment was higher in SIV-infected macaques than in uninfected animals. However, changes in LFA-1 levels were similar in both groups. These data show that LFA-1 surface levels are affected by pertussis toxin in vivo and this change may account in part, for the ability of pertussis toxin to induce lymphocytosis.

体内百日咳毒素处理可降低粘附整合素白细胞功能抗原-1 (LFA-1)的表面表达。
在猕猴百日咳毒素治疗抑制淋巴细胞从血液外渗,并导致短暂的淋巴细胞增多和白细胞增多。我们检查了已知参与外渗过程的淋巴细胞粘附分子,以寻找百日咳毒素治疗效果的可能机制。LFA-1的两个亚基CD11a和CD18在百日咳毒素处理动物的淋巴细胞表面表达低于未处理动物。粘附分子CD44和整合素VLA-4 α亚基(CD49d)未因百日咳毒素处理而降低。CD11a和CD18的低表面表达在所有淋巴细胞亚群中均可见,且与淋巴细胞增多程度呈负相关。siv感染的猕猴在百日咳毒素治疗后淋巴细胞增多的程度高于未感染的猕猴。然而,两组LFA-1水平的变化相似。这些数据表明,体内LFA-1表面水平受到百日咳毒素的影响,这种变化可能部分解释了百日咳毒素诱导淋巴细胞增多的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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