CD155 is expressed on cells of hematopoietic origin and by endothelial vessels inside secondary lymphoid organs including HEV. Upon activation, dendritic cells, T and B cells upregulate the surface level of CD155. CD155 is an ~45kD member of a subfamily of immunoglobulin-like adhesion receptors. Nectin 1-4 are other members of this subfamily, functioning in cell-cell contact by forming heterophilic and hemophilic trans-dimers. In contrast to nectins, CD155 lacks self adhesion potential but can interact with other nectins. This way, CD155 contributes in the formation of adherens junctions between endothelial and epithelial cells. Due to this adhesive capacity, CD155 influences processes such as cell motility, migration, growth, and formation of adherens junctions. Furthermore, CD155 is involved in immunological processes such as CD8 T cell-mediated tumor rejection, and NK cell-mediated killing. Many tumor types display an aberrant up-regulation of CD155 making them vulnerable to destruction by NK or cytotoxic T cells. In human, poliovirus, vitronectin and several other cellular receptors were identified as ligands that bind to CD155. CD96 (TACTILE) and CD226 (DNAM-1), both members of the Ig-superfamily, are other ligands of human CD155. Murine CD155 does not serve as a functional poliovirus receptor, however, murine CD155 recognizes the same panel of ligands like nectin-3, CD96, CD226 and vitronectin. CD155-deficient mice develop normally, however, a reduced humoral immune response to antigens entering the organism via the gastrointestinal tract is shown.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.