Abstract
Junctional Adhesion Molecule (JAM)-B is known as one of the members of the immunoglobulin super family and is involved in formation of tight junction of many types of cells including epithelial and endothelial cells. It has recently been demonstrated that, in response to inflammation, JAM-B present on the surface of endothelial cell forms heterophilic interactions with JAM-C on the leukocyte during transmigration from blood vessels into affected tissues. The formation of JAM-B－JAM-C complex strongly suggests that this heterophilic interaction plays an important role in the transmigration of the leukocytes. To address this question, I generated mice lacking JAM-B. Subsequently, I examined leukocyte transmigration in JAM-B−/− mice by Contact Hyper Sensitivity (CHS) model using oxazolone as sensitizing agent and thioglycollate-induced peritonitis model. From these analyses, I found that levels of leukocyte transmigration in JAM- B−/− mice were similar to those of wild - type mice. Thus, our results established that the gene is dispensable for this event.
