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Mol. Life Sci."],"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>A breach of T cell tolerance is considered as a major step in the pathogenesis of rheumatoid\u00a0arthritis. In collagen-induced arthritis (CIA) model, immunization with type II collagen (COL2) leads to arthritis in mice through T cells responding to the immunodominant COL2<jats:sub>259\u2013273<\/jats:sub> peptide. T cells could escape from thymus negative selection because endogenous COL2<jats:sub>259\u2013273<\/jats:sub> peptide only weakly binds to the major histocompatibility complex class II (MHCII) molecule A<jats:sup>q<\/jats:sup>. To investigate the regulation of T cell tolerance, we used a new mouse strain BQ<jats:italic>.Col2<\/jats:italic><jats:sup><jats:italic>266E<\/jats:italic><\/jats:sup> with homozygous D266E mutations in the <jats:italic>Col2<\/jats:italic> gene leading to a replacement of the endogenous aspartic acid (D) to glutamic acid (E) at position 266 of the COL2<jats:sub>259\u2013273<\/jats:sub> peptide, resulting in stronger binding to A<jats:sup>q<\/jats:sup>. We also established BQ<jats:italic>.Col2<\/jats:italic><jats:sup><jats:italic>264R<\/jats:italic><\/jats:sup> mice carrying an additional K264R mutation changed the lysine (K) at position 264 to eliminate the major TCR recognition site. The BQ<jats:italic>.Col2<\/jats:italic><jats:sup><jats:italic>266E<\/jats:italic><\/jats:sup> mice were fully resistant to CIA, while the BQ<jats:italic>.Col2<\/jats:italic><jats:sup><jats:italic>264R<\/jats:italic><\/jats:sup> mice developed severe arthritis. Furthermore, we studied two of the most important non-MHCII genes associated with CIA, i.e., <jats:italic>Ncf1<\/jats:italic> and <jats:italic>Fcgr2b.<\/jats:italic> Deficiency of either gene induced arthritis in BQ<jats:italic>.Col2<\/jats:italic><jats:sup><jats:italic>266E<\/jats:italic><\/jats:sup> mice, and the downstream effects differ as <jats:italic>Ncf1<\/jats:italic> deficiency reduced Tregs and was\u00a0likely to decrease expression of autoimmune regulator (AIRE) while <jats:italic>Fcgr2b<\/jats:italic> did not. In conclusion, the new human-mimicking mouse model has strong T cell tolerance to COL2, which can be broken by deficiency of <jats:italic>Fcgr2b<\/jats:italic> or <jats:italic>Ncf1<\/jats:italic>, allowing activation of autoreactive T cells and development of arthritis.<\/jats:p>","DOI":"10.1007\/s00018-022-04501-0","type":"journal-article","created":{"date-parts":[[2022,8,14]],"date-time":"2022-08-14T03:19:01Z","timestamp":1660447141000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Two major genes associated with autoimmune arthritis, Ncf1 and Fcgr2b, additively protect mice by strengthening T cell tolerance"],"prefix":"10.1007","volume":"79","author":[{"given":"Qijing","family":"Li","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianghong","family":"Zhong","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huqiao","family":"Luo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vilma","family":"Urbonaviciute","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhongwei","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chang","family":"He","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rikard","family":"Holmdahl","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2022,8,14]]},"reference":[{"key":"4501_CR1","doi-asserted-by":"publisher","first-page":"10","DOI":"10.1038\/s41590-020-00816-x","volume":"22","author":"CM Weyand","year":"2021","unstructured":"Weyand CM, Goronzy JJ (2021) The immunology of rheumatoid arthritis. 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