ABSTRACT
Lymphocyte migration is an essential requirement for efficient defense against infectious pathogens and for the recruitment of effector cells at sites of injury or infection. Recirculation of T-cells is precisely regulated by the controlled expression of a set of adhesion molecules on both the T-cells and the endothelial cells. Although leukocyte trafficking functions in immune surveillance, inappropriate trafficking to extravascular locations can lead to serious tissue injury and destruction. A role of inappropriate T-cell skin homing has been suggested in the initiation and perpetuation of the inflammatory process of skin diseases.1,2 The concept that T-cells play a pivotal role in many inflammatory disorders, such as psoriasis, contact dermatitis, or atopic dermatitis, has been corroborated in human diseases as well as in numerous animal models.3-6 Indeed, the number of T-cells infiltrating the skin has been correlated with disease activity that was demonstrated most elegantly for psoriasis.7
Therefore, interfering with the multistep process directing T-cells into the cutaneous compartments appears to be an attractive target to treat inflammatory skin diseases, an approach that is pursued by several pharmaceutical companies. In this review, we first try to identify interesting molecular targets that drive T-cells to inflamed skin. Next, we try to summarize efforts to interfere with these proteins aiming to
