Leukocyte adhesion deficiency (LAD) a rare primary immunodeficiency is due to defects in the leucocyte adhesion process. The phagocytes reach the site of inflammation to remove the pathogen.
A sequence of events such as marginalization, extravasations and movement to the site of inflammation through chemotaxis take place before the final action of phagocytes.
Defect in any one or more of these events affect the whole function of phagocytes. LAD is a failure to express CD18 a surface marker which forms the complement receptor protein for C3b on lymphocytes, macrophages, and neutrophils. Complement receptor protein is essential in adhesion for different lymphocytes.
An autosomal genetic defect results in defective production and also functions of this protein molecule. Since the adhesion of phagocytes to the capillary endothelial cells near the site of infection is necessary to develop effective inflammatory response, failure in the adhesion results in impaired function of not only phagocytes but also NK cells and T cells.