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The deficient mice present a mega\u2010oesophagus and have altered airway responsiveness. In addition, the number of circulating granulocytes is increased in\n                    <jats:italic>Jam\u2010C<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice as compared to control animals. These phenotypes probably reflect the different functions of JAM\u2010C expressed by endothelial and mesenchymal cells. Indeed, the deregulation in the number of circulating granulocytes is caused by the lack of JAM\u2010C expression on endothelial cells since rescuing endothelial expression of the protein in the\n                    <jats:italic>Jam\u2010C<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice is sufficient to restore homeostasis. More importantly, the rescue of vascular JAM\u2010C expression is accompanied by better survival of deficient mice, suggesting that endothelial expression of JAM\u2010C is mandatory for animal survival from opportunistic infections and fatal pneumonia. Copyright \u00a9 2007 Pathological Society of Great Britain and Ireland. 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