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

Summary 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.