Marked differences in Betapapillomavirus DNA and antibody prevalence between patients with psoriasis and those with atopic dermatitis.

BACKGROUND: Recent studies revealed that Betapapillomavirus (betaPV) infections are highly prevalent. Skin diseases such as psoriasis, characterized by keratinocyte hyperproliferation, and atopic dermatitis (AD), dominated by cutaneous inflammation, might have an impact on viral life cycle and immune response induction. OBJECTIVES: To investigate whether betaPV infection is different in psoriasis and AD. METHODS: Twenty-seven patients with psoriasis and 17 with AD were included for betaPV genotyping using eyebrow hairs, and for seroresponse determination. RESULTS: BetaPV DNA was found significantly more often in patients with psoriasis than in those with AD (100% vs. 81%, P=0·022) and the mean number of betaPV types was higher (4·8 vs. 2·1 types, P=0·002). In contrast, the seroprevalence in patients with AD was significantly higher compared with that in patients with psoriasis (88% vs. 56%, P=0·023). Type-specific concordance of serological response to the betaPV type detected in eyebrow hairs was 27% in patients with psoriasis and 47% in those with AD (P=0·019). CONCLUSIONS: We speculate that the condition of the skin and the immunological state of the patients have an important impact on the life cycle of betaPV.

Ultraviolet-A (UVA-1) radiation suppresses immunoglobulin production of activated B lymphocytes in vitro.

Previous studies have shown that low-dose ultraviolet-A (UVA-1) total body irradiations were capable of improving disease activity in patients with systemic lupus erythematosus (SLE). We hypothesized that UVA-1-induced suppression of immunoglobulin production by activated B cells in the dermal capillaries could be (partly) responsible for this effect. Our experiments with donor skin demonstrated that approximately 40% of UVA-1 could penetrate through the epidermis. Irradiation of peripheral blood mononuclear cells (PBMCs) with 2 J/cm(2) of UVA-1 resulted in 20% cell death. This toxic effect could be prevented totally by preincubation of the cell cultures with catalase. This indicates that the generation of hydrogen peroxide plays a role in UVA-1 cytotoxicity. T cells and B cells appeared to be less susceptible to UVA-1 cytotoxicity than monocytes. With the use of a CD40-CD40L B cell activation method we measured immunoglobulin production after various doses of UVA-1 irradiation (0-2 J/cm(2)). The doses of 2 J/cm(2) caused a significant decrease of IgM, IgG, IgA and IgE production under the conditions of interleukin (IL)-10 or IL-4 (IgE) stimulation. Although UVA-1 can cause apoptosis of B lymphocytes, we show that relatively low doses of UVA-1 radiation also affect the function of these cells. Both effects may be responsible for the observed improvement of disease activity in SLE patients.

Efficacy of UVA-1 cold light as an adjuvant therapy for systemic lupus erythematosus.

OBJECTIVE: The assessment of the efficacy of therapy of patients with moderately active systemic lupus erythematosus (SLE) with low doses of UVA-1 cold light. METHODS: A double blind, placebo-controlled, cross-over study design was used for the examination of the efficacy of low doses of UVA-1 radiation (12 J/cm2/day for 15 days) in 12 patients. RESULTS: UVA-1 treatment resulted in a significant decrease of well-validated disease activity indexes [the SLE Activity Measure (SLAM) (P < 0.001) and the SLE Disease Activity Index (SLEDAI) (P = 0.007)], whereas neither score improved significantly during placebo treatment. Furthermore, UVA-1 therapy proved to be more effective [mean decrease 4.8 points) than placebo (mean decrease -1.7 points (i.e. an increase)] when measured by the SLAM (P = 0.001, 95% CI -7.56 to -2.28), but not by the SLEDAI. Two patients had transient skin reactions at the beginning of treatment. CONCLUSION: UVA-1 therapy appears to be a useful adjuvant treatment modality for patients suffering from moderately active SLE. Its effect could possibly be explained by reduction of B-cell function or apoptosis of plasma cells.

A double-blind placebo-controlled trial of UVA-1 in the treatment of dyshidrotic eczema.

We carried out a randomized, double-blind, placebo-controlled study to examine the therapeutic effect of UVA-1 irradiation on dyshidrotic hand eczema. Twenty-eight patients were randomised to receive UVA-1 irradiation (40 J/cm2) or placebo, five times a week for 3 weeks. Evaluated by the DASI and the VAS, UVA-1 was significantly more effective after 2 and 3 weeks. Also, desquamation and area of affected skin improved significantly more after UVA-1. We did not find any difference regarding the response of patients with increased IgE blood levels (>100 IU/mL) compared with those having normal IgE levels. No side effects were observed. This study indicates that UVA-1 can cause a significant improvement of both objective and subjective signs of dyshidrotic eczema.