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We hypothesized that intercellular communication, mediated by extracellular vesicles, contributes to systemic juvenile idiopathic arthritis pathogenesis and that the number and cellular sources of extracellular vesicles would differ between inactive and active states of systemic juvenile idiopathic arthritis and healthy controls. We evaluated plasma from healthy pediatric controls and patients with systemic juvenile idiopathic arthritis with active systemic flare or inactive disease. We isolated extracellular vesicles by size exclusion chromatography and determined total extracellular vesicle abundance and size distribution using microfluidic resistive pulse sensing. Cell-specific extracellular vesicle subpopulations were measured by nanoscale flow cytometry. Isolated extracellular vesicles were validated using a variety of ways, including nanotracking and cryo-electron microscopy. Extracellular vesicle protein content was analyzed in pooled samples using mass spectrometry. Total extracellular vesicle concentration did not significantly differ between controls and patients with systemic juvenile idiopathic arthritis. Extracellular vesicles with diameters &amp;lt;200 nm were the most abundant, including the majority of cell-specific extracellular vesicle subpopulations. Patients with systemic juvenile idiopathic arthritis had significantly higher levels of extracellular vesicles from activated platelets, intermediate monocytes, and chronically activated endothelial cells, with the latter significantly more elevated in active systemic juvenile idiopathic arthritis relative to inactive disease and controls. Protein analysis of isolated extracellular vesicles from active patients showed a proinflammatory profile, uniquely expressing heat shock protein 47, a stress-inducible protein. Our findings indicate that multiple cell types contribute to altered extracellular vesicle profiles in systemic juvenile idiopathic arthritis. The extracellular vesicle differences between systemic juvenile idiopathic arthritis disease states and healthy controls implicate extracellular vesicle\u2013mediated cellular crosstalk as a potential driver of systemic juvenile idiopathic arthritis disease activity.<\/jats:p>","DOI":"10.1093\/jleuko\/qiad059","type":"journal-article","created":{"date-parts":[[2023,5,18]],"date-time":"2023-05-18T23:53:36Z","timestamp":1684454016000},"page":"387-403","source":"Crossref","is-referenced-by-count":7,"title":["Extracellular vesicles in systemic juvenile idiopathic arthritis"],"prefix":"10.1093","volume":"114","author":[{"given":"Justine","family":"Maller","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine , 269 Campus Drive, CCSR Rm 2105c, Stanford, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terry","family":"Morgan","sequence":"additional","affiliation":[{"name":"Departments of Pathology and Biomedical Engineering, Oregon Health & Sciences University , 3181 SW Sam Jackson Portland, OR 97239 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mayu","family":"Morita","sequence":"additional","affiliation":[{"name":"Departments of Pathology and Biomedical Engineering, Oregon Health & Sciences University , 3181 SW Sam Jackson Portland, OR 97239 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"McCarthy","sequence":"additional","affiliation":[{"name":"Chan Zuckerberg Biohub , 265 Campus Drive, Palo Alto, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunshin","family":"Jung","sequence":"additional","affiliation":[{"name":"Department of Pathology, Stanford University School of Medicine , 300 Pasteur Dr, Edwards R238, Stanford, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrin J","family":"Svensson","sequence":"additional","affiliation":[{"name":"Department of Pathology, Stanford University School of Medicine , 300 Pasteur Dr, Edwards R238, Stanford, CA 94305 , United States"},{"name":"Stanford Diabetes Research Center , Stanford, CA 94305 , United States"},{"name":"Stanford Cardiovascular Institute , Stanford, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua E","family":"Elias","sequence":"additional","affiliation":[{"name":"Chan Zuckerberg Biohub , 265 Campus Drive, Palo Alto, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5472-8086","authenticated-orcid":false,"given":"Claudia","family":"Macaubas","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine , 269 Campus Drive, CCSR Rm 2105c, Stanford, CA 94305 , United States"},{"name":"Department of Pediatrics, Program in Immunology, Stanford University School of Medicine , 269 Campus Drive, CCSR Rm 2105c, Stanford, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Mellins","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine , 269 Campus Drive, CCSR Rm 2105c, Stanford, CA 94305 , United States"},{"name":"Department of Pediatrics, Program in Immunology, Stanford University School of Medicine , 269 Campus Drive, CCSR Rm 2105c, Stanford, CA 94305 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,5,18]]},"reference":[{"issue":"7","key":"2023102617152921100_qiad059-B1","doi-asserted-by":"crossref","first-page":"416","DOI":"10.1038\/nrrheum.2011.68","article-title":"Pathogenesis of systemic juvenile idiopathic arthritis: some answers, more questions","volume":"7","author":"Mellins","year":"2011","journal-title":"Nat Rev Rheumatol"},{"key":"2023102617152921100_qiad059-B2","doi-asserted-by":"crossref","first-page":"101632","DOI":"10.1016\/j.smim.2022.101632","article-title":"The clinical heterogeneity of adult onset Still's Disease may underlie different pathogenic mechanisms. 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