Endothelial cells and adhesion molecules in experimental autoimmune encephalomyelitis

Abstract

Under normal circumstances, entry of immune system cells into the central nervous system (CNS) is restricted by the blood-CNS barrier. However, with activation, cells of the immune system undergo changes that allow for an immune response within the CNS. The animal model, experimental autoimmune encephalomyelitis (EAE), is an important tool by which to investigate these processes. Using EAE, it has been shown that the establishment of an immune response in the CNS involves activation not only of the infiltrating inflammatory cells, but also of the CNS endothelial cells. Receptor-ligand interactions between CNS-EC and invading immune cells involved in EAE are multi-factorial. Particularly critical interactions occur between cell surface selectins on leukocytes and addressins on CNS-EC, and between integrins on leukocytes and their ligands on CNS-EC and other CNS cells. These interactions are good targets for potential therapies of MS, the human disease for which EAE is a model.