Leukocyte adhesion in host defense and tissue injury

During their life span, leukocytes adhere transiently to one another, to other cell types, such as vascular endothelial cells, and to extracellular matrix proteins. This adhesiveness is mediated by families of specific cell surface adhesion molecules, namely, integrins, immunoglobulin superfamily molecules, and selectins. Adhesion is required for leukocyte-mediated cytotoxicity, phagocytosis, chemotaxis, and induction of lymphocyte proliferation and maturation. It also participates in recirculation and homing of lymphocytes into lymphoid organs and in leukocyte migration from the vascular compartment to extravascular tissues. Adhesion underlies the beneficial or detrimental role of leukocytes in immune and inflammatory responses. In animals, blocking monoclonal antibodies to adhesion molecules dramatically reduce vascular and tissue injury in several organs following ischemia-reperfusion, and delay renal allograft rejection. Moreover, expression of particular adhesion molecules is induced or increased in cells which are targets for allergic or autoimmune reactions and in inflamed tissues. On the other hand, a congenital deficiency of the CD11/CD18 integrins (Leu-CAMs) leads to recurrent, and sometimes fatal, bacterial infections, and lack of particular cell-adhesion molecules on Burkitt's lymphoma cells may enable these cells to escape immunosurveillance.