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This review examines Still\u2019s disease through this spectrum lens, integrating recent advances in pathogenesis, clinical heterogeneity, and therapeutic approaches.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Findings<\/jats:title>\n                    <jats:p>Emerging mechanistic insights reveal complex innate-adaptive immune interactions. Type I interferon signalling and neutrophil extracellular trap formation drive inflammation, while hyperferritinemia actively perpetuates disease through Msr1-mediated signaling. mTORC1 has emerged as a central integration hub converging multiple cytokine signals. Adaptive mechanisms increasingly contribute to complications: both macrophage activation syndrome and lung disease demonstrate IFN\u03b3-dominant pathology with T cell hyperactivation. Clinical phenotyping identifies distinct patient clusters\u2014from hyperferritinemic monocyclic to catastrophic multiorgan phenotypes\u2014reflecting varying innate-adaptive contributions. Current classification criteria permit considerable diagnostic latitude and may inadvertently group mechanistically distinct conditions under a single diagnostic label. IL-1 and IL-6 receptor blockade remain therapeutic cornerstones, with evidence supporting early intervention during a window of opportunity. Novel approaches including IL-18 binding protein, JAK inhibitors, and IFN\u03b3 blockade show promise in refractory disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>Still's disease predominantly reflects autoinflammatory pathology driven by innate immune dysregulation, yet adaptive mechanisms contribute meaningfully to disease heterogeneity and complications. Recognition as a spectrum disorder\u2014with variable innate-adaptive contributions across patients and disease phases\u2014supports unification of pediatric and adult forms, guides mechanistically targeted therapies, and emphasizes the need for biomarker-driven patient stratification to enable personalized treatment approaches.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11926-026-01210-6","type":"journal-article","created":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T09:10:24Z","timestamp":1770023424000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Still\u2019s Disease and Autoinflammation: Positioning an Inflammatory Syndrome on the Autoinflammation-Autoimmunity Spectrum"],"prefix":"10.1007","volume":"28","author":[{"given":"Daniel","family":"Pietsch","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sinisa","family":"Savic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,2]]},"reference":[{"issue":"8","key":"1210_CR1","doi-asserted-by":"publisher","first-page":"e297","DOI":"10.1371\/journal.pmed.0030297","volume":"3","author":"D McGonagle","year":"2006","unstructured":"McGonagle D, McDermott MF. 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