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Deficient RNA Editing Implicated in Inflammatory Disease 

Genetic variants that reduce the editing levels of double-stranded RNA are associated with autoimmune and immune-mediated conditions, a study finds.

Written byAlejandra Manjarrez, PhD
| 3 min read
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Following transcription, RNA molecules can undergo modifications. For example, nucleotides may be inserted, deleted, or changed. One of the most common edits, which new research shows plays an important role in the onset of inflammatory disease, is the transformation of the nucleotide adenosine into inosine within a double-stranded RNA. A study published Wednesday (August 3) in Nature reveals that genetic variants that dampen this specific modification are associated with an increased risk of autoimmune and immune-mediated inflammatory disorders such as psoriasis, inflammatory bowel disease, and type 1 diabetes. The authors propose that a sensor protein likely mistakes these less-edited RNAs for foreign molecules, triggering an inflammatory response.

“I think it’s really a major breakthrough,” says Mary A. O’Connell, a molecular biologist at the Central European Institute of Technology at Masaryk University in the Czech Republic who did not participate in this study but has previously collaborated with some of the ...

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Meet the Author

  • alejandra manjarrez

    Alejandra Manjarrez is a freelance science journalist who contributes to The Scientist. She has a PhD in systems biology from ETH Zurich and a master’s in molecular biology from Utrecht University. After years studying bacteria in a lab, she now spends most of her days reading, writing, and hunting science stories, either while traveling or visiting random libraries around the world. Her work has also appeared in Hakai, The Atlantic, and Lab Times.

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