ABSTRACT
Adhesive interactions are critical for the effective functioning of normal immune responses. It is, therefore, not surprising that aberrant cell adhesion lies at the heart of many pathological processes, such as inflammation, tumour growth and metastasis, and autoimmunity. Normal immune responses depend on the right cells interacting with each other in the right place at the right time. Most pathological process result, at least in part, because of perturbations in leukocyte activation and adhesion, leading to the wrong cell accumulating in the wrong place at the wrong time. Tremendous progress has been made in the last decade in defining the molecular basis of T cell adhesion and its importance in T cell recognition and migration, and this has led to the development of novel therapeutic targets. In addition, the interdependence of adhesion and apoptosis for the effective resolution of immune responses has been demonstrated at the molecular level by the finding that a number of adhesion molecules play an important role in the recognition and clearance of apoptotic cells by phagocytic cells (1). Ultimately, effective host defense requires effective cross-talk between the regulatory proteins involved in the inflammatory and complement cascades, cells of the immune system and resident tissue stromal cells, such as interstitial macrophages and fibroblasts. To illustrate the critical role of adhesion receptors in the immunopathogenesis of autoimmune diseases, we will highlight their role in leukocyte adhesion, activation and endothelial transmigration. We have emphasized these features of T cell adhesion molecules partly because they are the ones about which most is known, and partly because they are unique to leukocytes.
