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© The Rockefeller University Press, 0022-1007/1999/2/711/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 4, February 15, 1999 711-718


Articles

312-nanometer Ultraviolet B Light (Narrow-Band UVB) Induces Apoptosis of T Cells within Psoriatic Lesions

Maki Ozawa, Katalin Ferenczi, Toyoko Kikuchi, Irma Cardinale, Lisa M. Austin, Todd R. Coven, Lauren H. Burack, and James G. Krueger

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.

Key Words: psoriasis • immunosuppression • T lymphocyte • apoptosis • ultraviolet light


Address correspondence to James G. Krueger, Laboratory for Investigative Dermatology, The Rockefeller University, 1230 York Ave., New York, NY 10021-6399. Phone: 212-327-7730; Fax: 212-327-8232; E-mail: kruegej{at}rockvax.rockefeller.edu

This research was supported in part by a General Clinical Research Center Grant (M01-RR00102) from the National Center for Research Resources at the National Institutes of Health; by National Institutes of Health grant AI39214; and by grants or gifts from The Carl J. Herzog Foundation, the American Skin Association, The Carson Family Charitable Trust, Dr. James Murphy, and Jean Stein. L.H. Burack and T.R. Coven were supported as Rockefeller University Clinical Scholars from May 1996 through June 1997 and March 1997 through June 1998, respectively.

Abbreviations used: AnV, Annexin V; APC, allophycocyanin; BB, broad band; FSC, forward scatter; NB, narrow band; PerCP, peridinine chlorophyll protein; PI, propidium iodide; SSC, side scatter; TUNEL, terminal deoxynucleotidyl transferase–mediated dUTP-biotin nick end labeling.


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