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Rheumatology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study aims to characterize pathogenic somatic mutations in patients with autoinflammatory or autoimmune diseases lacking disease\u2010causing germline mutations, explore their contribution to disease pathogenesis and progression, and evaluate their implications for diagnosis and targeted therapy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed a systematic analysis of somatic mutations in a selected panel of 185 immune\u2010related genes in 2,912 patients with autoinflammatory or autoimmune diseases, recruited from 41 medical centers across China, who were previously negative for germline mutations based on whole\u2010exome sequencing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified both previously reported and novel somatic mutations in genes such as\n                      <jats:italic>UBA1<\/jats:italic>\n                      ,\n                      <jats:italic>KRAS<\/jats:italic>\n                      , and\n                      <jats:italic>NLRP3<\/jats:italic>\n                      . Pathogenic somatic mutations in\n                      <jats:italic>TNFAIP3<\/jats:italic>\n                      were discovered first in patients with autoinflammatory diseases. The pathogenic somatic mutation detection rate was 1.35% in adults and 0.97% in children, emphasizing the importance of genetic diagnosis and novel gene discovery for somatic mutations. In addition, somatic mutations in Ras\u2010related genes were identified in seven patients, and 39 clonal hematopoiesis\u2013associated mutations were identified in 36 adult patients. Moreover, myeloid cells harboring somatic mutations expanded during disease flare and reduced during remission. Disregarding the dynamic elevation of the variant allele fraction during disease progression led to therapeutic failure.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study delineated the genetic landscape of pathogenic somatic mutations underlying autoinflammatory and autoimmune diseases, offering valuable insights for genetic diagnosis and targeted therapies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.70126","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T14:35:41Z","timestamp":1773066941000},"page":"1975-1988","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Landscape of Somatic Mutations in a Large Cohort of Chinese Patients With Immune Dysregulations"],"prefix":"10.1002","volume":"78","author":[{"given":"Jinjian","family":"Fu","sequence":"first","affiliation":[{"name":"Life Sciences Institute, Zhejiang University, Department of Rheumatology, The Second Affiliated Hospital, Zhejiang University School of Medicine  Hangzhou China"},{"name":"Liangzhu Laboratory of Zhejiang University  Hangzhou China"},{"name":"Department of Rheumatology Sir Run Run Shaw Hospital, Zhejiang University School of Medicine  Hangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiong","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Rheumatology Renji Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"Shanghai Immune Therapy Institute  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Wang","sequence":"additional","affiliation":[{"name":"Liangzhu Laboratory of Zhejiang University  Hangzhou 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