In LAD I the firm adhesion of leukocyte to the endothelium is defective, because of mutations in the gene encoding the beta(2)-integrin.
LAD II involved the first phase, rolling phase, and is caused by mutations in the specific fucose transporter to the Golgi apparatus.
LAD III is the last syndrome to be described and a primary activation defect in all three beta-integrins 1, 2, and 3 is detected.
The most recent discovery is mutations in kindlin 3, a newly recognized component, which binds the cytoplasmic tail of integrin.
Rolling Adhesion. This video describes the way in which leukocytes bind to the blood vessel endothelium. This video is from: Janeway's Immunobiology, 7th Edition Murphy, Travers, & Walport. Source: Garland Science.
Leukocyte adhesion defects in Oxford handbook of clinical immunology and allergy By Gavin Spickett:
Updates on genetic etiologies of leukocyte adhesion defects. http://bit.ly/sygq6
Leukocyte adhesion deficiency (LAD)
CD15, Sialyl LewisX (SLeX)