{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T03:49:07Z","timestamp":1790480947077,"version":"4.1.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T00:00:00Z","timestamp":1736208000000},"content-version":"vor","delay-in-days":1467,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The human MHC class II molecule HLA-DQ2.5 is implicated in multiple autoimmune disorders, including celiac disease, type 1 diabetes, and systemic lupus erythematosus. The pathogenic contribution of HLA-DQ2.5 in many of these disorders is not fully understood. There is thus a need for an HLA-DQ2.5 humanized mouse model with physiological expression of this MHC molecule that can be integrated into disease models. In this article, we report the generation of an HLA-DQ2.5 knock-in mouse strain on a C57BL\/6 background in which sequences encoding the extracellular moieties of mouse MHC class II H2-IAa and H2-IAb1 have been replaced with those of HLA-DQA1*05:01 and HLA-DQB1*02:01. In heterozygous knock-in mice, the expression of HLA-DQ2.5 is superimposable with the expression of H2-IA. This was not the case in a regular untargeted HLA-DQ2.5 transgenic mouse. HLA-DQ2.5 in the knock-in animals is functional for T cell development and for Ag presentation to HLA-DQ2.5\u2013restricted and gluten-specific T cells. Because C57BL\/6 mice do not express H2-IEa, the only functional MHC class II molecule in homozygous HLA-DQ2.5 knock-in mice is the knock-in gene product. This alleviates the need for crossing with MHC class II knockout mice to study the isolated function of the MHC transgene. Our novel mouse strain provides an important tool to study the involvement of HLA-DQ2.5 in models of diseases with association to this HLA allotype.<\/jats:p>","DOI":"10.4049\/immunohorizons.2000107","type":"journal-article","created":{"date-parts":[[2021,1,18]],"date-time":"2021-01-18T16:30:56Z","timestamp":1610987456000},"page":"25-32","source":"Crossref","is-referenced-by-count":15,"title":["Generation of an HLA-DQ2.5 Knock-In Mouse"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7314-5778","authenticated-orcid":false,"given":"Alisa E","family":"Dewan","sequence":"first","affiliation":[{"name":"KG Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo , 0372 Oslo ,","place":["Norway"]},{"name":"Department of Immunology, Oslo University Hospital-Rikshospitalet , 0372 Oslo ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5660-4028","authenticated-orcid":false,"given":"Frank","family":"Koentgen","sequence":"additional","affiliation":[{"name":"Ozgene Pty. Ltd. , Bentley, Western Australia 6983 ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4501-4222","authenticated-orcid":false,"given":"Marie K","family":"Johannesen","sequence":"additional","affiliation":[{"name":"KG Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo , 0372 Oslo ,","place":["Norway"]},{"name":"Department of Immunology, Oslo University Hospital-Rikshospitalet , 0372 Oslo ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9231-643X","authenticated-orcid":false,"given":"M Fleur","family":"du Pre","sequence":"additional","affiliation":[{"name":"KG Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo , 0372 Oslo ,","place":["Norway"]},{"name":"Department of Immunology, Oslo University Hospital-Rikshospitalet , 0372 Oslo ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8860-704X","authenticated-orcid":false,"given":"Ludvig M","family":"Sollid","sequence":"additional","affiliation":[{"name":"KG Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo , 0372 Oslo ,","place":["Norway"]},{"name":"Department of Immunology, Oslo University Hospital-Rikshospitalet , 0372 Oslo ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,1,19]]},"reference":[{"key":"2025010703473856600_r1","volume-title":"HLA in Health and Disease.","author":"Lechler","year":"2000"},{"key":"2025010703473856600_r2","doi-asserted-by":"crossref","first-page":"257","DOI":"10.1111\/j.1600-065X.1999.tb01398.x","article-title":"The genetic basis for the association of the 8.1 ancestral haplotype (A1, B8, DR3) with multiple immunopathological diseases","volume":"167","author":"Price","year":"1999","journal-title":"Immunol. 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