Research press release


Nature Medicine

Signals of solar injury


UVBに曝されると日焼けが起こり、炎症や損傷につながる。Richard Galloたちは、UVBによって皮膚細胞が損傷を受けると、損傷した特殊なRNAが細胞から放出されることを明らかにした。UVB照射されていない皮膚細胞や血液中の免疫細胞がこのRNAを感知すると、炎症誘発因子の分泌が起こる。自然免疫応答を作動させるToll様受容体3(TLR3)をもたないマウスでは、炎症分子が分泌されず、皮膚がそれほど赤くならないことから、UVB損傷による炎症応答には、この受容体が必要なことがわかる。


RNAs damaged by ultraviolet B radiation (UVB) causes inflammation and injury of the skin, reports a new study published online this week in Nature Medicine. Recognition of these RNAs by the immune system and skin cells could be blocked to treat photosensitive disorders.

Inflammation and injury result from sunburn caused upon exposure to UVB. Richard Gallo and colleagues show that damage of skin cells by UVB leads to the release of a specific form of damaged RNA from these cells. This RNA is then sensed by unirradiated skin cells and immune cells in the blood, causing secretion of proinflammatory factors. Mice lacking the receptor toll-like receptor 3 (TLR3), which mediates innate immune responses, failed to secrete the inflammatory molecules and showed less redness, indicating that the inflammatory response caused by UVB damage is dependent on this receptor.

Although other products formed after UVB exposure can contribute to inflammation and further testing in humans is needed, the findings suggest that RNAs from damaged skin cells can serve as signals of solar injury.

doi: 10.1038/nm.2861


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