E-cadherin is best characterized as adherens junction protein, which through homotypic interactions contributes to the maintenance of the epithelial barrier function. In epithelial cells, the cytoplasmic tail of E-cadherin forms a dynamic complex with catenins and regulates several intracellular signal transduction pathways, including Wnt/β-catenin, PI3K/Akt, Rho GTPase, and NF-κB signaling. Recent progress uncovered a novel and critical role for this adhesion molecule in mononuclear phagocyte functions. E-cadherin regulates the maturation and migration of Langerhans cells, and its ligation prevents the induction of a tolerogenic state in bone marrow-derived dendritic cells (DCs). In this respect, the functionality of β-catenin could be instrumental in determining the balance between immunogenicity and tolerogenicity of DCs in vitro and in vivo. Fusion of alternatively activated macrophages and osteoclasts is also E-cadherin-dependent. In addition, the E-cadherin ligands CD103 and KLRG1 are expressed on DC-, T-, and NK-cell subsets and contribute to their interaction with E-cadherin-expressing DCs and macrophages. Here we discuss the regulation, function, and implications of E-cadherin expression in these central orchestrators of the immune system.
|Titolo:||Regulation and function of the E-cadherin/catenin complex in cells of the monocyte-macrophage lineage and DCs|
|Parole Chiave:||Macrophages ; Animals ; Dendritic Cells ; Cell Lineage ; Humans ; beta Catenin ; Cell Differentiation ; Cadherins ; Models, Biological ; Multiprotein Complexes ; Monocytes ; Signal Transduction ; Immune System|
|Settore Scientifico Disciplinare:||Settore MED/04 - Patologia Generale|
|Data di pubblicazione:||16-feb-2012|
|Digital Object Identifier (DOI):||10.1182/blood-2011-10-384289|
|Appare nelle tipologie:||01 - Articolo su periodico|