Platelet endothelial cell adhesion molecule deficiency or blockade significantly reduces leukocyte emigration in a majority of mouse strains
Platelet endothelial cell adhesion molecule deficiency or blockade significantly reduces leukocyte emigration in a majority of mouse strains
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DOI：
10.4049/jimmunol.173.10.6403
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发表时间：
2004-11-15
影响因子：
4.4
通讯作者：
Muller, WA
中科院分区：
文献类型：
--
作者：
Schenkel, AR;Chew, TW;Muller, WA
PECAM是一种专门在中性粒细胞和单核细胞离开血液室时的渗出步骤中使用的分子。抗PECAM试剂，如Ab和可溶性融合蛋白，在体内和体外均阻断渗出。然而，C57 BL/6品系中的PECAM敲除小鼠在大多数炎症模型中没有严重缺陷。我们在这项研究中表明，在两种炎症模型中，相同的PECAM敲除与FVB/n菌株回交明显减少了白细胞迁移。此外，我们表明，抗PECAM试剂可以阻止白细胞迁移在几个其他野生型品系的小鼠，如FVB/n，SJL，和远交品系瑞士韦伯斯特。这清楚地表明，C57 BL/6菌株能够独特地补偿PECAM功能的丧失。应使用FVB/n或其他小鼠品系重新评估已使用C57 BL/6小鼠研究的炎性疾病的鼠类模型，以确定PECAM是否在这些模型中发挥作用。
PECAM is a molecule used specifically during the diapedesis step when neutrophils and monocytes leave the blood compartment. Anti-PECAM reagents, such as Abs and soluble fusion proteins, block diapedesis both in vivo and in vitro. However, the PECAM knockout mouse in C57BL/6 strain has no serious defects in most models of inflammation. We show in this study that the same PECAM knockout backcrossed into the FVB/n strain clearly has reduced leukocyte emigration in two models of inflammation. Furthermore, we show that anti-PECAM reagents can block leukocyte emigration in several other wild-type strains of mice like FVB/n, SJL, and the outbred strain Swiss Webster. This clearly shows that the C57BL/6 strain is uniquely able to compensate for the loss of PECAM function. Murine models of inflammatory disease that have been studied using C57BL/6 mice should be re-evaluated using FVB/n or other mouse strains to determine whether PECAM plays a role in those models.