We have developed preliminary data which establishes that 312 nm UVB is more clinically effective than conventional UVB sources in the treatment of psoriasis. The precise cellular mechanism of 312 nm UVB has not been established, but it most likely relates to direct immunosuppressive effects on activated leukocytes in psoriatic skin lesions or on circulating immune cells. In preliminary experiments we have found that 312 nm UVB induces T-cell apoptosis after high level exposure and T-cell anergy after low-level exposure (with evidence of both effects in irradiated psoriatic skin lesions). However, of even more importance, we have found that 312 nm may produce systemic immune suppression, inducing T-lymphocyte anergy and/or apoptosis in circulating cells. Observations that 312 nm UVB could have major effects on systemic immune function have been made on only limited numbers of patients in our clinical trials and must be confirmed by more extensive and complete studies. Hence, we will conduct a formal clinical trial to compare the relative immune modulating effects of 312 nm UVB vs. conventional UVB, when given in therapeutically relevant dosing regimens, on 1) pathologic immune activation in diseased skin, 2) cutaneous immune function in unaffected skin regions, and 3) systemic cellular immunity mediated by circulating T-lymphocytes.
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