Xenon chloride ultraviolet B laser is more effective in treating psoriasis and in inducing T cell apoptosis than narrow-band ultraviolet B

Abstract

Earlier we reported that a 308-nm xenon chloride (XeCl) UVB laser is highly effective for treating psoriasis. As ultraviolet B light seems to cause T cell apoptosis, in the present study we studied the ability of the XeCl laser to induce T-cell apoptosis in vitro, and then compared the apoptosis-inducing capacities of narrow-band UVB (NB-UVB) light and the XeCl laser. The role of laser impulse frequency and intensity in the therapeutical and apoptosis-inducing efficacy of XeCl laser was also investigated. Both XeCl laser and NB-UVB induced T cell apoptosis, but quantitative induction was greater with XeCl laser. Changes in the frequency and intensity of impulses of XeCl laser did not influence its therapeutic and T cell apoptosis-inducing efficacy. These results suggest that the more effective induction of T cell apoptosis can be responsible for the greater clinical efficacy of XeCl laser compared to NB-UVB. Additionally, the optical properties of the XeCl laser (a monochromatic, coherent, pulse-mode laser; easier precise dosimetry, there are no ‘contaminating’ wavelengths) can make this laser light an ideal tool for studies of the mode of action of UVB light.

Introduction

Psoriasis vulgaris is a chronic inflammatory skin disease that affects 2–3% of the population. Ultraviolet B (UVB) light (290–320 nm) is a widely used therapeutic modality for the disease. Initially, broad-band (BB)-UVB light sources were applied which emit wavelengths throughout the whole spectrum of UVB light. An action spectrum study in patients with psoriasis established that at wavelengths from 304 to 313 nm suberythemogenic exposure doses resulted in complete clearing, while wavelengths from 290 to 300 nm produced the sunburn reaction, but had no therapeutic benefit [1]. These findings led to the introduction of the narrow-band (NB)-UVB light source in the therapy; this also emits polychromatic light, but the 311–313 nm wavelength range predominates in its emission spectrum. In a bilateral comparative study, NB-UVB light proved superior to BB-UVB for the treatment of psoriasis [2].

Xenon chloride (XeCl) UVB laser treatment is a new and promising form of therapy for psoriasis vulgaris [3], because all of its energy is emitted within the action spectrum for the phototherapy of psoriasis (Fig. 1). This laser emits its total energy at 308 nm and may therefore be regarded as a ‘super narrow band’ UVB light source. We demonstrated earlier that the cumulative dose required for the complete clearance of psoriatic plaques is six times less with the XeCl laser than with NB-UVB therapy [3]. The high clinical efficacy of the XeCl laser for psoriasis was later confirmed by other studies [4], [5]. The clinical efficacy of the XeCl laser in psoriasis is therefore well documented, but the mechanism of its high efficacy has not been investigated so far.

There is considerable evidence, that psoriasis vulgaris is mediated by activated T-lymphocytes infiltrating the epidermis and the dermo-epidermal interface [6]. The major mechanism of action of UVB light in the treatment of inflammatory dermatoses is the cytotoxic effect on the infiltrating T-cells, where the mechanism of cell death is most probably apoptosis. NB-UVB light has been found to be a more potent inductor of T-cell apoptosis than BB-UVB light, therefore, the T-cell apoptosis-inducing capacity of a UVB light source can be paralleled by its clinical efficacy [7].

In the present study, we investigated whether changes of the light intensity and impulse frequency of the XeCl laser influence its therapeutic efficacy. As UVB light seems to cause T-cell apoptosis, we studied the ability of the XeCl laser to induce T-cell apoptosis in vitro, and then compared the apoptosis-inducing capacities of NB-UVB light and the XeCl laser.