The normal inflammatory response to infections requires the peripheral leukocytes to migrate across the blood vessels to the site of infection in response to chemotactic factors released in the site. The importance of cell to cell adhesion between the leukocytes and vascular endothelial cells in the leukocyte migration across the blood vessels was substantiated by the finding of a recently defined heritable disease called leukocyte adhesion deficiency (LAD). LAD is a disorder characterized by recurrent bacterial infections, impaired pus formation and wound healing, persistent periodontitis, and an abnormally high peripheral leukocyte count. The profound pathogenesis of the LAD has been defined as impairments in adhesion-dependent leukocyte functions such as chemotaxis due to a lack of leukocyte cell-surface expression of adhesion molecules of LFA-1, Mac-1 and p150/95, the beta 2-integrin. Very recently, a new disorder having almost the same clinical features and leukocyte dysfunctions as the LAD but normal expression of the beta 2-integrin was identified. The disease lacks cell-surface carbohydrate components, the sialyl Lewis antigens which are the ligands of another kind of adhesion molecule of selectins expressed on the vascular endothelial cells. The presence of these two diseases indicates that the leukocyte locomotion requires cell to cell adhesion through both the beta 2-integrin and selectins.