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Background  Pathogenic immune responses are known to play an important role in abdominal aortic aneurysm ( AAA ) development. Ultraviolet B ( UVB ) irradiation has been demonstrated to have therapeutic potential not only for cutaneous diseases but also for systemic inflammatory diseases in mice by suppressing immunoinflammatory responses. We investigated the effect of  UVB  irradiation on experimental  AAA .    Methods and Results  We used an angiotensin  II –induced  AAA  model in apolipoprotein E–deficient mice fed a high‐cholesterol diet. Mice aged 10 weeks were irradiated with 5 kJ/m 2   UVB  once weekly for 6 weeks ( UVB ‐irradiated, n=38; nonirradiated, n=42) and were euthanized for evaluation of  AAA  formation at 16 weeks. Overall, 93% of angiotensin  II –infused mice developed  AAA , with 60% mortality possibly because of aneurysm rupture.  UVB  irradiation significantly decreased the incidence (66%) and mortality (29%) of  AAA  ( P =0.004 and  P =0.006, respectively).  UVB ‐irradiated mice had significantly smaller diameter  AAA  ( P =0.008) and fewer inflammatory cells in the aortic aneurysm tissue than nonirradiated mice, along with systemic expansion of  CD 4 + Foxp3 +  regulatory T cells and decreased effector  CD 4 +  CD 44 high  CD 62L low  T cells in para‐aortic lymph nodes. Genetic depletion of regulatory T cells abrogated these beneficial effects of  UVB  treatment, demonstrating a critical role of regulatory T cells.    Conclusions  Our data suggest that  UVB ‐dependent expansion of regulatory T cells has beneficial effects on experimental  AAA  and may provide a novel strategy for the treatment of  AAA .

Ultraviolet B Exposure Inhibits Angiotensin II –Induced Abdominal Aortic Aneurysm Formation in Mice by Expanding CD 4 + Foxp3 + Regulatory T Cells