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- Publisher
- Wiley
- Copyright
- Copyright © 2007 Wiley Subscription Services
- ISSN
- 0022-3417
- eISSN
- 1096-9896
- DOI
- 10.1002/path.2163
- pmid
- 17455169
- Publisher site
- See Article on Publisher Site
Abstract
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. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Journal
The Journal of Pathology – Wiley
Published: Jan 1, 2007
Keywords: ; ; ;