Abstract
Lymphocytes are in a dynamic state of flux moving from the blood stream into lymphoid and extralymphoid tissues and eventually returning to the general circulation. This continuous process permits the full repertoire of lymphocyte specificities to be available for immune reactions. The regulation of lymphocyte traffic to specific tissue locations is complex and involves lymphocyte-endothelial interactions at sites of extravasation. Some of the molecules involved in lymphocyte-endothelial adhesion interactions have now been cloned and sequenced using molecular biology techniques. Lymphocyte migration to chronic inflammatory sites such as rheumatoid synovium shares a number of similarities to that involved in normal organized lymphoid tissue. First, at sites of chronic disease there are marked morphological changes to the vascular endothelium resulting in high endothelial venules identical to those found in normal lymphoid tissue. In addition, there are functional changes in vascular endothelial behavior that are receptor-mediated and regulate lymphocyte traffic to inflamed sites. The nature of these molecules on endothelial cells (addressins) and the regulation of their expression is still unclear. The control of lymphocyte migration appears to be influenced by selective lymphocyte-endothelial recognition in both health and inflammatory disease. The factors that modulate these interactions are reviewed.
Published Version
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