{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:11:02Z","timestamp":1791846662663,"version":"4.3.4"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,6,15]],"date-time":"2016-06-15T00:00:00Z","timestamp":1465948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004359","name":"Vetenskapsr\u00e5det","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007435","name":"\u00c5ke Wiberg Stiftelse","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007435","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004063","name":"Knut och Alice Wallenbergs Stiftelse","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004063","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Various rodent models of arthritis are essential to dissect the full complexity of human rheumatoid arthritis (<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>), a common autoimmune disease affecting joints. The <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content> model of arthritis originates from a spontaneous mutation in <jats:styled-content style=\"fixed-case\">ZAP<\/jats:styled-content>\u201070 found in a <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c colony. This mutation affects T cell selection due to reduced <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content> signalling, which allows leakage of self\u2010reactive T cells from the thymus. To further expand the practical applicability of this unique model in arthritis research, we investigated the arthritogenicity of the <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content> mutation in two common black mouse strains C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6.Q and C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/10.Q and compared to <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c.Q. Mice retained the reduced <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content> signalling characteristic of <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content>.<jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice, which leads to similar alteration in thymic selection. Importantly, mice also retained susceptibility to chronic arthritis after a single injection of mannan from <jats:italic>Saccharomyces cerevisiae<\/jats:italic>, with comparable prevalence and severity regardless of the genetic background. Further characterization of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells revealed a similar bias towards <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production and activated T cell phenotype in all <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content> strains compared to respective wild type controls. Finally, transfer of <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content> thymocytes conferred susceptibility to recipients, which confirm the intrinsic defect and pathogenicity of T cells. Overall, these results underline the strong impact that the W163C <jats:styled-content style=\"fixed-case\">ZAP<\/jats:styled-content>\u201070 mutation has on T cell\u2010driven arthritis, and they support the use of the <jats:styled-content style=\"fixed-case\">SKG<\/jats:styled-content> model in black mice, which is useful for further investigations of this distinctive arthritis model to better understand autoimmunity.<\/jats:p>","DOI":"10.1111\/sji.12438","type":"journal-article","created":{"date-parts":[[2016,4,4]],"date-time":"2016-04-04T11:14:14Z","timestamp":1459768454000},"page":"3-11","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["The <scp>SKG<\/scp> Mutation in <scp>ZAP<\/scp>\u201070 also Confers Arthritis Susceptibility in C57 Black Mouse Strains"],"prefix":"10.1111","volume":"84","author":[{"given":"S.","family":"Guerard","sequence":"first","affiliation":[{"name":"Division of Medical Inflammation Research Department of Medical Biochemistry and Biophysics Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Boieri","sequence":"additional","affiliation":[{"name":"Institute of Basic Medical Sciences Faculty of Medicine University of Oslo Oslo Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Hultqvist","sequence":"additional","affiliation":[{"name":"Division of Medical Inflammation Research Department of Medical Biochemistry and Biophysics Karolinska Institutet Stockholm Sweden"},{"name":"Redoxis AB Medicon Village Scheelev\u00e4gen 2 Lund Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Holmdahl","sequence":"additional","affiliation":[{"name":"Division of Medical Inflammation Research Department of Medical Biochemistry and Biophysics Karolinska Institutet Stockholm 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