BASIC MECHANISM OF LEUKOCYTE MIGRATION

Inflammation represents the consequence of capillary dilation with acc umulation of fluid (edema) and the immigration of leukocytes. By the e nd of the last century, Metchnikoff noted the power of certain blood c ells to move toward bacteria and foreign substances and ingest them. I n fact, leukocytes adhere to the vascular endothelium, and subsequentl y leave the circulation by transendothelial migration driven by chemoa ttractants, a process known as diapedesis. Reversible adherence of leu kocytes to endothelium, basement membranes, and other surfaces on whic h they crawl is an essential event in the establishment of inflammatio n, whose molecular basis is beginning to be understood. Inflammation c an become chronic. The acute process, characterized by neutrophil infi ltration and edema, gives way to a subsequent predominance of mononucl ear phagocytes or lymphocytes. Insulin-dependent diabetes mellitus is the result of organ-specific autoimmune destruction of the insulin sec reting p-cells in the pancreatic islets of Langerhans. It has become e vident that diabetes mellitus is a multifactorial disease caused in pa rt by infiltrating T-lymphocytes, comparable to situations of inflamma tion. After presentation of the different effecters of the immune syst em and their fluxes through the body, this review will propose a gener al model of adhesion between leukocytes and endothelial cells. It will emphasize how the homing specificity of lymphocyte subsets to differe nt lymphoid organs is ensured, and how leukocyte migration to sites of inflammation is regulated, Finally, general therapeutic perspectives based on adhesion molecules leading to cure or prevention of chronic i nflammation will be discussed.