Abstract
AIM: Our previous studies identified ultraviolet B (UVB) irradiation as a possible approach for preventing atherosclerosis. The aim of this study was to clarify the effect of 312 nm UVB, a wavelength similar to that of clinically available narrow-band UVB for the treatment of psoriasis, on atherosclerosis and the underlying mechanisms. METHODS AND RESULTS: Using a recently developed UVB-light-emitting diode device, we irradiated 6-week-old male atherosclerosis-prone apolipoprotein E-deficient mice with 312 nm UVB at 5 or 10 kJ/m² and examined its effect on the development of atherosclerosis and immunoinflammatory responses by performing histological analysis, flow cytometry, biochemical assays, and liquid chromatography/mass spectrometry-based lipidomics. UVB irradiation at 10 kJ/m² but not at 5 kJ/m² significantly attenuated the development of aortic root atherosclerotic plaques, while UVB irradiation at both doses induced a less inflammatory plaque phenotype. This atheroprotective effect was associated with a reduced effector T cell number, a shift toward anti-atherogenic helper T cell responses, and increased proportion of regulatory T cells in lymphoid tissues and increased levels of proresolving lipid mediators in the skin. CONCLUSIONS: We demonstrated that 312 nm UVB irradiation limits atherosclerosis by favorably modulating the T cell balance and lipid mediator profile. Our findings indicate that 312 nm UVB phototherapy could be an attractive immunomodulatory approach for preventing and treating atherosclerosis.