“…Although these patients had a persistent leukocytosis, very few leukocytes accumulated at infected, necrotic lesions. In 1984 several groups demonstrated that these patients' leukocytes were missing CDt la,b,c/CD18 and subsequent work has demonstrated that the primary genetic defects are in CD18, the shared subunit (2)(3)(4)(5)23,24). Thus, the inability of leukocytes to adhere to endothelium or other particles because of an inherited defect in adhesive molecules prevents accumulation of leukocytes at sites of microbial invasion and results in severe, recurrent infections.…”