ABSTRACT
The interaction of endothelial and tissue-based adhesion molecules with their respective ligands on circulating mononuclear cells mediates their adherence to sites of inflammation. Adhesion molecules also regulate leukocyte circulation, lymphoid tissue homing, endothelial accumulation, transendothelial migration, and persistence of effector cells in the extracellular matrix. These adhesive interactions, at several levels and due to various causes, mediate sequestration and persistence of inflammatory cells and their associated cytokines to immune and autoimmune sites of inflammation. Conversely, modulation or blockade of these molecules appears to ameliorate autoimmune disease, particularly in experimental models. Modulation of adhesive forces include, but are likely not limited to, changes in adhesion molecule avidity with activation, cytokine stimulation, surface expression and density, progression of temporal expression, and circulating soluble ligands (1,2).
