Loss of cadherin-11 in atherosclerosis immune response: altered macrophage migration and T cell activation

The objective of this study was to understand the impact of losing cadherin-11 (CDH11) on the immune response in atherosclerosis. CDH11 has previously been demonstrated to be associated with a number of fibrotic diseases, but its exact role in inflammation remains relatively unknown. In vivo models of atherosclerosis demonstrated altered immune cell profiles with CDH11-deficiency, including decreased circulating myeloid cell populations. In vitro studies of CDH11-deficient macrophages revealed increased expression of genes associated with migration, despite a functional decrease in migration, possibly due to compensatory mechanisms. RNAseq analysis also showed increased expression of MHC class II molecule genes in CDH11-/- macrophages, indicating that loss of CDH11 in macrophages could alter T cell populations through increased activation of CD4+ helper T cells. These results together indicate that CDH11 can alter the immune response, in part by impairing macrophage migration and by affecting T cell activation. Macrophages were collected from the bone marrow of 3 WT controls and 4 CDH11-/- experimental animals. Macrophages were differented in L929 conditioned media for 7 days in vitro prior to total RNA collection.