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J. Exp. Med.,
Volume 189, Number 4, February 15, 1999 711-718
By
From the Laboratory for Investigative Dermatology, The Rockefeller University, New York
10021-6399
Narrow-band (312 nm) ultraviolet B light (UVB) is a new form of therapy for psoriasis, but its
mechanism of action is unknown. In a bilateral comparison clinical study, daily exposure of
psoriatic plaques to broad-band UVB (290-320 nm) or 312-nm UVB depleted T cells from the
epidermis and dermis of psoriatic lesions. However, 312-nm UVB was significantly more depleting in both tissue compartments. To characterize the mechanism of T cell depletion, assays
for T cell apoptosis were performed on T cells derived from UVB-irradiated skin in vivo and
on T cells irradiated in vitro with 312-nm UVB. Apoptosis was induced in T cells exposed to
50-100 mJ/cm2 of 312-nm UVB in vitro, as measured by increased binding of fluorescein isothiocyanate (FITC)-Annexin V to CD3+ cells and by characteristic cell size/granularity
changes measured by cytometry. In vivo exposure of psoriatic skin lesions to 312-nm UVB for
1-2 wk also induced apoptosis in T cells as assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) reaction in tissue sections, by binding of FITC-Annexin V to CD3+ T cells contained in epidermal cell suspensions, and by detection of apoptosis-related size shifts of CD3+ cells. Induction of T cell apoptosis could be the
main mechanism by which 312-nm UVB resolves psoriasis skin lesions.
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