{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T20:52:12Z","timestamp":1784667132767,"version":"3.55.0"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,1,28]],"date-time":"2019-01-28T00:00:00Z","timestamp":1548633600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Korean Health Technology R&D Project"},{"name":"Ministry for Health & Welfare, Republic of Korea","award":["HI14C1894"],"award-info":[{"award-number":["HI14C1894"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CR<\/jats:styled-content>6\u2010interacting factor 1 (<jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1) is a nuclear protein that interacts with other nuclear factors and androgen receptors, and is implicated in the regulation of cell cycle progression and cell growth. In this study, we examined whether CRIF1 exerts an immunoregulatory effect by modulating the differentiation and function of pathogenic T cells. To this end, the role of <jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 in rheumatoid arthritis, a systemic autoimmune disease characterized by hyperplasia of synovial tissue and progressive destruction of articular cartilage structure by pathogenic immune cells [such as T helper type 17 (Th17) cells], was investigated. p3<jats:styled-content style=\"fixed-case\">XFLAG<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">CMV<\/jats:styled-content>\u201010\u2010<jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 was administered to mice with collagen\u2010induced arthritis 8 days after collagen type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> immunization and the disease severity and histologic evaluation, and osteoclastogenesis were assessed. <jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 over\u2010expression in mice with collagen\u2010induced arthritis attenuated the clinical and histological signs of inflammatory arthritis. Furthermore, over\u2010expression of <jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 in mice with arthritis significantly reduced the number of signal transducer and activator of transcription 3\u2010mediated Th17 cells in the spleen as well as osteoclast differentiation from bone marrow cells. To investigate the impact of loss of <jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 in T cells, we generated a conditional <jats:styled-content style=\"fixed-case\">CRIF<\/jats:styled-content>1 gene ablation model using <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4\u2010cre transgenic mice and examined the frequency of Th17 cells and regulatory T cells. Deficiency of CRIF1 in <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> cells promoted the production of interleukin\u201017 and reduced the frequency of regulatory T cells. These results suggest a role for CRIF1 in modulating the activities of Th17 cells and osteoclasts in rheumatoid arthritis.<\/jats:p>","DOI":"10.1111\/imm.13042","type":"journal-article","created":{"date-parts":[[2018,12,26]],"date-time":"2018-12-26T12:44:15Z","timestamp":1545828255000},"page":"413-421","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["CR6\u2010interacting factor 1 controls autoimmune arthritis by regulation of signal transducer and activator of transcription 3 pathway and T helper type 17 cells"],"prefix":"10.1111","volume":"156","author":[{"given":"Jin\u2010Sil","family":"Park","sequence":"first","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Si\u2010Young","family":"Choi","sequence":"additional","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun\u2010Hee","family":"Hwang","sequence":"additional","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung\u2010Min","family":"Kim","sequence":"additional","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JeongWon","family":"Choi","sequence":"additional","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South 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University of Korea Seoul South Korea"},{"name":"Department of Medical Life Science College of Medicine The Catholic University of Korea Seoul Korea"},{"name":"Department of Biomedicine &amp; Health Sciences, College of Medicine The Catholic University of Korea Seoul Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung\u2010Hwan","family":"Park","sequence":"additional","affiliation":[{"name":"The Rheumatism Research Center Catholic Research Institute of Medical Science The Catholic University of Korea Seoul South Korea"},{"name":"Divison of Rheumatology Department of Internal Medicine The Catholic University of Korea Seoul South 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