{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T02:05:37Z","timestamp":1780106737073,"version":"3.54.0"},"reference-count":31,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2003,4,1]],"date-time":"2003-04-01T00:00:00Z","timestamp":1049155200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mitochondrial DNA is subject to increased rates of mutations due to its proximity to the source of reactive oxygen species. Here we show that increased MHC class I (MHC I) expression serves to alert the immune system to cells with mitochondrial mutations. MHC I is overexpressed in fibroblasts with mitochondrial dysfunction from patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes and in lymphocytes from purine nucleoside phosphorylase-deficient immune-deficient mice with mitochondrial DNA deletions. Consistent with a role of MHC I in the elimination of cells containing mitochondrial DNA mutations, mice deficient in MHC I accumulate mitochondrial DNA deletions in various tissues. These observations in both mice and humans suggest a role for the immune system in preventing reversion of mitochondrial DNA back into a parasitic state following deleterious mutations affecting mitochondrial oxidative phosphorylation.<\/jats:p>","DOI":"10.4049\/jimmunol.170.7.3603","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:28:40Z","timestamp":1398022120000},"page":"3603-3607","source":"Crossref","is-referenced-by-count":18,"title":["Role of MHC Class I in Immune Surveillance of Mitochondrial DNA Integrity"],"prefix":"10.1093","volume":"170","author":[{"given":"Yiping","family":"Gu","sequence":"first","affiliation":[{"name":"Division of Immunology and Allergy, Departments of Pediatrics and Immunology, Infection, Immunity, Injury, and Repair Program, Research Institute, University of Toronto and Hospital for Sick Children , Toronto, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunjie","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Immunology and Allergy, Departments of Pediatrics and Immunology, Infection, Immunity, Injury, and Repair Program, Research Institute, University of Toronto and Hospital for Sick Children , Toronto, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chaim M","family":"Roifman","sequence":"additional","affiliation":[{"name":"Division of Immunology and Allergy, Departments of Pediatrics and Immunology, Infection, Immunity, Injury, and Repair Program, Research Institute, University of Toronto and Hospital for Sick Children , Toronto, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amos","family":"Cohen","sequence":"additional","affiliation":[{"name":"Division of Immunology and Allergy, Departments of Pediatrics and Immunology, Infection, Immunity, Injury, and Repair Program, Research Institute, University of Toronto and Hospital for Sick Children , Toronto, Ontario ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,4,1]]},"reference":[{"key":"2026020210081773700_R1","first-page":"871","volume-title":"J. 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