Research ArticleCYTOKINES

The m6A reader IMP2 directs autoimmune inflammation through an IL-17– and TNFα-dependent C/EBP transcription factor axis

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Science Immunology  02 Jul 2021:
Vol. 6, Issue 61, eabd1287
DOI: 10.1126/sciimmunol.abd1287

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IL-17 makes its m6A marks

IL-17 and related cytokines not only support host defense against certain pathogens but also contribute to the development of autoimmune diseases. A holistic understanding of how IL-17 initiates and propagates inflammation is needed to identify additional therapeutic opportunities in autoimmunity. Bechara et al. probed the role of N6-methyladenosine (m6A) modifications of IL-17–induced transcripts in enhancing their stability and translation. Epitranscriptomic m6A marks were detected on the mRNAs for the C/EBPβ and C/EBPδ transcription factors involved in IL-17 signaling. The noncanonical m6A reader protein IMP2 was implicated in binding these m6A marks. Mice lacking IMP2 were less susceptible to an autoantibody-induced model of kidney disease driven by IL-17 signaling. These findings establish posttranscriptional modifications of mRNAs involved in proinflammatory cytokine signaling as potential targets for therapeutic intervention.

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