A class of genetic regulators called microRNAs can directly influence the severity of inflammatory diseases reports a study published online this week in Nature Medicine. Moreover, an inflammatory response can be amplified by turning off microRNAs, pointing to novel ways to decrease damaging inflammatory responses by influencing genetic regulatory programs.
Increased amounts of the cytokine interleukin-17 (IL-17) are found in several autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis. This cytokine promotes inflammatory damage by influencing the development of circulating immune cells. Youcun Qian and colleagues found that IL-17 can also contribute to this damage by suppressing a specific microRNA called miR-23b in cells residing in tissues. IL-17 amounts were elevated in the kidney and joint of individuals with systemic lupus erythematosus and rheumatoid arthritis, respectively, whereas the expression of miR-23b was decreased. The authors found a direct relationship between these two molecules in three mouse models of autoimmune disease-lupus, rheumatoid arthritis and multiple sclerosis-with IL-17 reducing the expression of miR-23b. Its overexpression, in turn, blocked autoimmune disease development in these mouse models.
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