Ultraviolet-A (UVA-1) radiation suppresses immunoglobulin production of activated B lymphocytes in vitro
Autor: | C. van Kooten, N. P. M. Smit, S. Pavel, S.W. Kamerling, M. C. A. Polderman |
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Jazyk: | angličtina |
Rok vydání: | 2006 |
Předmět: |
Ultraviolet Rays
T-Lymphocytes Immunology Immunoglobulins Immunoglobulin E Lymphocyte Activation Peripheral blood mononuclear cell Monocytes Tissue Culture Techniques Basic Immunology Immunology and Allergy Medicine Humans Lupus Erythematosus Systemic Cytotoxicity Skin B-Lymphocytes Epidermis (botany) biology Cell Death business.industry Interleukin Dose-Response Relationship Radiation Catalase Interleukin-10 Apoptosis Cell culture biology.protein sense organs Interleukin-4 Antibody business |
Popis: | SummaryPrevious 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/cm2 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/cm2). The doses of 2 J/cm2 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. |
Databáze: | OpenAIRE |
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