Signals of solar injury

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.