The role of the immune system in the pathogenesis of psoriasis.
 Psoriatic involved skin contains an increased number of activated T cells.
 The mechanism through which these T cells achieve and maintain their activated state is unknown, and both antigen-dependent and -independent mechanisms may contribute.
 Recently a novel pathway of antigen-independent T-cell activation has been described.
 This pathway is identified by a monoclonal antibody that binds to a T-cell membrane surface molecule termed "UM4D4.".
 This molecule is expressed on a minority (20%) of psoriatic peripheral blood T cells but on a majority (75%) of the T cells in lesional skin.
 Thus, UM4D4 could play a role in antigen-independent T-cell activation in psoriasis.
 Indeed the monoclonal antibody anti-UM4D4 consistently induces proliferation of psoriatic UM4D4+ T-cell clones.
 The activity of antigen-dependent pathways are also enhanced in psoriatic epidermis in as much as involved skin relative to uninvolved skin contains an increased number and function of antigen-presenting cells.
 Upon activation, the lesional T cells release lymphokines.
 Central to the immune hypothesis of psoriasis is that some of these T-cell lymphokines act on keratinocytes to induce changes characteristic of psoriasis.
 Indeed lymphokines from lesional psoriatic T-cell clones directly alter in vitro keratinocyte phenotype through induction of intercellular adhesion molecule-1 (ICAM-1) and HLA-DR cell-surface expression.
 Furthermore, the lymphokines also enhance keratinocyte growth.
 These data suggest a critical role for the immune system in the pathogenesis of psoriasis.
