ABSTRACT
Immunological studies have vastly improved our understanding of the pathogenesis of psoriasis. It is now clear that psoriasis results from an immunological response that involves multiple T-cell-mediated events (1, 2). A key element in the initiation and maintenance of this chronic disease involves T-cell activation. Full T-cell activation requires two events (3). The first involves presentation of antigen bound to the major histocompatibility complex (MHC) on the surface of the antigen-presenting cell (APC) to a T-cell receptor (TCR). The second is stabilization of the APC-T cell interaction through binding of secondary receptor-ligand pairs to form an immunological synapse (4).
