INFLAMMATORY AND IMMUNE-RESPONSES ARE IMPAIRED IN MICE DEFICIENT IN INTERCELLULAR-ADHESION MOLECULE-1
INFLAMMATORY AND IMMUNE-RESPONSES ARE IMPAIRED IN MICE DEFICIENT IN INTERCELLULAR-ADHESION MOLECULE-1
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DOI：
10.1073/pnas.90.18.8529
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发表时间：
1993-09-15
影响因子：
11.1
通讯作者：
BEAUDET, AL
中科院分区：
文献类型：
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作者：
SLIGH, JE;BALLANTYNE, CM;BEAUDET, AL
基因打靶用于产生细胞间粘附分子 1 (ICAM-1) 或 CD54 缺陷的小鼠，CD54 是一种结合 β2 整联蛋白的免疫球蛋白样细胞粘附分子。纯合缺陷动物发育正常，具有生育能力，并且具有中度粒细胞增多症。突变的性质、RNA 分析和免疫染色与 ICAM-1 表面表达的完全丧失一致。缺陷小鼠表现出明显的炎症反应异常，包括化学性腹膜炎导致的中性粒细胞迁移受损以及对 2,4-二硝基氟苯的接触超敏反应降低。突变细胞在混合淋巴细胞反应中提供的刺激可以忽略不计，尽管它们作为反应细胞正常增殖。这些突变动物对于研究 ICAM-1 及其反受体在炎症性疾病过程和动脉粥样硬化中的作用非常有价值。
Gene targeting was used to produce mice deficient in intercellular adhesion molecule 1 (ICAM-1) or CD54, an immunoglobulin-like cell adhesion molecule that binds beta2 integrins. Homozygous deficient animals develop normally, are fertile, and have a moderate granulocytosis. The nature of the mutation, RNA analysis, and immunostaining are consistent with complete loss of surface expression of ICAM-1. Deficient mice exhibit prominent abnormalities of inflammatory responses including impaired neutrophil emigration in response to chemical peritonitis and decreased contact hypersensitivity to 2,4-dinitrofluorobenzene. Mutant cells provided negligible stimulation in the mixed lymphocyte reaction, although they proliferated normally as responder cells. These mutant animals will be extremely valuable for examining the role of ICAM-1 and its counterreceptors in inflammatory disease processes and atherosclerosis.