Leukocyte trafficking from the bloodstream to tissue is important for the continuous surveillance of foreign antigens, as well as for rapid leukocyte accumulation at sites of inflammatory response or tissue injury. Leukocyte emigration to sites of inflammation is a dynamic process, involving multiple steps in an adhesion cascade. Various adhesion molecules are expressed on both resting and stimulated endothelial cells and leukocytes.
Defects in a number of these adhesion molecules result in recognized clinical syndromes. Three leukocyte adhesion deficiency (LAD) syndromes have been delineated and a fourth category of newly-described defects will be reviewed :
●LAD I, in which the beta 2 integrin family is deficient or defective
●LAD II, in which the fucosylated carbohydrate ligands for selectins are absent
●LAD III, in which activation of all beta integrins (1, 2, and 3) is defective