http://atvb.ahajournals.org/content/37/1/66?etoc=
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Visual Overview
Abstract
Objective—UVB
irradiation is an established treatment for immunoinflammatory
cutaneous disorders and has been shown to suppress cutaneous and
systemic inflammatory diseases through modulation of the adaptive immune
response. However, it remains unknown whether UVB irradiation prevents
an immunoinflammatory disease of arteries such as atherosclerosis.
Approach and Results—Here,
we show that UVB exposure inhibits the development and progression of
atherosclerosis in atherosclerosis-prone mice by expanding and enhancing
the functional capacity of CD4+ forkhead box P3+
regulatory T cells and regulating proatherogenic T-cell responses.
Experimental studies in Langerhans cell–depleted mice revealed that
epidermal Langerhans cells play a critical role in UVB-dependent
induction of CD4+ forkhead box P3+ regulatory T cells, suppression of proatherogenic T-cell responses, and prevention of atherosclerotic plaque development.
Conclusions—Our
findings suggest the skin immune system as a novel therapeutic target
for atherosclerosis and provide a novel strategy for the treatment and
prevention of atherosclerosis.
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