ABSTRACT
In many inflammatory skin diseases, T cells accumulate around the dermal perivascular plexus and some subsequently migrate into the epidermis. These T cells are thought to make a major contribution to inflammation and tissue damage in these skin diseases. On the other hand, T cells residing in skin are supposed to play an important role in protecting the epidermis from potentially dangerous immune responses. In mice, a unique T-cell subset, namely dendritic epidermal γδ-TCR positive T cells (DETC), has been characterized as being responsible for the maintenance of immunologie homeostasis within skin, however, a human epidermotrophic T-cell analogue has not been identified as of yet (Shiohara and Moriya, 1997). Specialized antigen-presenting cells (APC) resident in skin, namely Langerhans cells, are considered to play a central role in the induction of T cellmediated cutaneous immune responses. Upon antigen-capture, i.e. by epicutaneously applied haptens or invading pathogens, these sentinel cutaneous APC migrate via dermal lymphatics into the T-cell areas of skin-draining lymphoid tissues where T cells are activated. Subsequently, these antigen-specific T cells travel via the blood stream to the original site of antigen-deposition. Also, cutaneous APC, i.e. Langerhans cells and dermal dendritic cells, are well equipped to stimulate resident T cells intracutaneously (Banchereau and Steinman, 1998). However, it must be noted that the integrated immune system within skin is not only comprised of a distinctive population of resident and recirculating T cells and cutaneous APC. Additionally, neighboring cells like keratinocytes, fibroblasts, and mast cells regulate T-cell responses via cytokine-mediated intercellular communication and cell-cell interactions (Takashima and Bergstresser, 1996). Thus, mechanisms of intracutaneous as well as extracutaneous T-cell activation are of central importance for the pathophysiology of inflammatory and some malignant skin diseases.
