UVB Exposure Prevents Atherosclerosis by Regulating Immunoinflammatory Responses

Ask your doctor to translate how much UVB radiation the mice were getting and how much comes from sunlight and map that to your body size. Will you need to join a nudist group and attend every weekend?
http://atvb.ahajournals.org/content/37/1/66?etoc=

Naoto Sasaki, Tomoya Yamashita, Kazuyuki Kasahara, Atsushi Fukunaga, Tomoyuki Yamaguchi, Takuo Emoto, Keiko Yodoi, Takuya Matsumoto, Kenji Nakajima, Tomoyuki Kita, Masafumi Takeda, Taiji Mizoguchi, Tomohiro Hayashi, Yoshihiro Sasaki, Mayumi Hatakeyama, Kumiko Taguchi, Ken Washio, Shimon Sakaguchi, Bernard Malissen, Chikako Nishigori, Ken-ichi Hirata

https://doi.org/10.1161/ATVBAHA.116.308063

Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:66-74

Originally published October 20, 2016

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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.