Imhof B A, Zimmerli C, Gliki G, Ducrest-Gay D, Juillard P, Hammel P, Adams R, Aurrand-Lions M
Department of Pathology and Immunology, Centre Médical Universitaire, 1 Rue Michel Servet, 1204, Geneva, Switzerland.
J Pathol. 2007 Jun;212(2):198-208. doi: 10.1002/path.2163.
Jam-C(-/-) mice exhibit growth retardation and multilobular pneumonia concomitant with poor survival of the mice under conventional housing conditions. The deficient mice present a mega-oesophagus and have altered airway responsiveness. In addition, the number of circulating granulocytes is increased in Jam-C(-/-) mice as compared to control animals. These phenotypes probably reflect the different functions of JAM-C expressed by endothelial and mesenchymal cells. Indeed, the deregulation in the number of circulating granulocytes is caused by the lack of JAM-C expression on endothelial cells since rescuing endothelial expression of the protein in the Jam-C(-/-) mice is sufficient to restore homeostasis. More importantly, the rescue of vascular JAM-C expression is accompanied by better survival of deficient mice, suggesting that endothelial expression of JAM-C is mandatory for animal survival from opportunistic infections and fatal pneumonia.
在传统饲养条件下，Jam-C基因敲除（Jam-C(-/-)）小鼠表现出生长发育迟缓、多叶性肺炎，同时小鼠存活率较低。这些缺陷小鼠出现巨食管，并伴有气道反应性改变。此外，与对照动物相比，Jam-C(-/-)小鼠循环粒细胞数量增加。这些表型可能反映了内皮细胞和间充质细胞表达的JAM-C的不同功能。事实上，循环粒细胞数量的失调是由于内皮细胞上缺乏JAM-C表达所致，因为在Jam-C(-/-)小鼠中恢复该蛋白的内皮表达足以恢复体内平衡。更重要的是，血管JAM-C表达的恢复伴随着缺陷小鼠更好的存活率，这表明JAM-C的内皮表达对于动物在机会性感染和致命性肺炎中存活至关重要。
