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NETs counteract microbes but are also linked to inflammation in atherosclerosis, arthritis, or psoriasis by unknown mechanisms. Here, we report that NET-associated RNA (naRNA) stimulates further NET formation in naive PMNs via a unique TLR8-NLRP3\u00a0inflammasome-dependent pathway. Keratinocytes respond to naRNA with expression of psoriasis-related genes (e.g.,\n                    <jats:italic>IL17, IL36<\/jats:italic>\n                    ) via atypical NOD2-RIPK signaling. In vivo, naRNA drives\u00a0temporary skin inflammation, which is drastically ameliorated by genetic ablation of RNA sensing. Unexpectedly,\u00a0the naRNA-LL37 \u2018composite damage-associated molecular pattern (DAMP)\u2019 is pre-stored in resting neutrophil granules, defining sterile NETs as inflammatory webs that amplify neutrophil activation. However, the activity of the naRNA-LL37 DAMP is transient and hence supposedly self-limiting under physiological conditions. Collectively,\u00a0upon dysregulated NET release like in psoriasis, naRNA sensing may represent both a potential cause of disease and a new intervention target.\n                  <\/jats:p>","DOI":"10.1038\/s44319-024-00150-5","type":"journal-article","created":{"date-parts":[[2024,5,23]],"date-time":"2024-05-23T05:01:59Z","timestamp":1716440519000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["naRNA-LL37 composite DAMPs define sterile NETs as self-propagating drivers of inflammation"],"prefix":"10.1038","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5073-4243","authenticated-orcid":false,"given":"Francesca","family":"Bork","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten 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