Structure and function of the leukocyte adhesion molecules CD11/CD18.

INCE THE EARLY studies of Metchnikoff in the S 1880s,’ a large body of data has been accumulated that established a crucial role for circulating polymorphonuclear leukocytes (PMN) in host defense against pyogenic infections.’*2 These studies also amply documented a pathogenic role for these cells in host tissue damage in many noninfectious diseases.2 The same cellular processes underlie this contribution of PMN to host defense and tissue destruction. Such processes include chemotaxis, phagocytosis, degranulation with release of many proteolytic enzymes, eicosanoid and prostanoid products, and production of superoxide anions and hydroxyl radicals. Although significant progress has been made in understanding the underlying basic mechanisms, a critical role for PMN adhesion in many of these processes and its profound biologic importance were only recently established. This was the direct result of a series of parallel studies, one aimed at generating monoclonal antibodies (MoAbs) to leukocyte surface antigens’.’ and characterizing these antigens, and the other aimed at elucidation of the cellular and molecular basis of an inherited immunodeficiency disease (Leu-CAMor CDll/CD18 deficiency), characterized by impaired leukocyte adhesion and recurrent and often fatal bacterial infection^?'^ These studies led to a recognition of a common relationship, through cell adhesion, between processes underlying both the beneficial and detrimental roles of PMN. These studies also established the critical role of CD11/CD18 leukocyte adhesion molecules in vivo and have generated novel means for controlling PMN-induced tissue injury. In this report, I will briefly review the structure, function, and biologic role of CD11/ CD18.