Impaired anaphylactic responses with intact sensitivity to endotoxin in mice lacking a platelet-activating factor receptor.
Impaired anaphylactic responses with intact sensitivity to endotoxin in mice lacking a platelet-activating factor receptor.
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在缺乏血小板激活因子受体的小鼠中，对内毒素具有完整敏感性的过敏反应受损。
DOI：
10.1084/jem.187.11.1779
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发表时间：
1998-06-01
影响因子：
15.3
通讯作者：
Shimizu, T
中科院分区：
文献类型：
--
作者：
Ishii, S;Kuwaki, T;Nagase, T;Maki, K;Tashiro, F;Sunaga, S;Cao, W H;Kume, K;Fukuchi, Y;Ikuta, K;Miyazaki, J;Kumada, M;Shimizu, T
血小板活化因子（PAF）是一种有效的磷脂介质，除了其众所周知的刺激血小板聚集的能力外，还具有多种生物活性。药理学研究表明PAF在妊娠、神经细胞迁移、过敏反应和内毒素休克中起作用。在这里，我们表明，破坏PAF受体基因在小鼠引起全身过敏症状显著减少。然而，出乎意料的是，缺乏PAF受体的小鼠发育正常，生育能力强，对细菌内毒素仍然敏感。这些突变小鼠清楚地表明，PAF在引起过敏反应中起主导作用，但对生殖、大脑发育或内毒素休克不是必需的。
Platelet-activating factor (PAF) is a potent phospholipid mediator with diverse biological activities in addition to its well-known ability to stimulate platelet aggregation. Pharmacologic studies had suggested a role for PAF in pregnancy, neuronal cell migration, anaphylaxis, and endotoxic shock. Here we show that disruption of the PAF receptor gene in mice caused a marked reduction in systemic anaphylactic symptoms. Unexpectedly, however, the PAF receptor–deficient mice developed normally, were fertile, and remained sensitive to bacterial endotoxin. These mutant mice clearly show that PAF plays a dominant role in eliciting anaphylaxis, but that it is not essential for reproduction, brain development, or endotoxic shock.