{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T08:52:20Z","timestamp":1791103940011,"version":"4.1.0"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2014,6,1]],"date-time":"2014-06-01T00:00:00Z","timestamp":1401580800000},"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":[[2014,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Endoplasmic reticulum\u2013associated aminopeptidase-1 (ERAP1) plays a critical role in the processing of peptides prior to binding to MHC class I molecules. In this article, we show for the first time, to our knowledge, that the HLA-B27 immunodominant influenza nucleoprotein (NP) 383\u2013391 epitope is made as an N-terminally extended 14-mer before it is trimmed by ERAP. In the absence of ERAP, there is a significant reduction in the CTL response to the B27\/NP383\u2013391 epitope in influenza A (flu)\u2013infected B27\/ERAP\u2212\/\u2212 mice. With the use of tetramer staining, the number of naive CD8+ T cells expressing TCR V\u03b28.1 in B27\/ERAP\u2212\/\u2212 transgenic mice is significantly lower than that seen in B27\/ERAP+\/+ mice. HLA-B27 surface expression in naive and flu-infected B27\/ERAP\u2212\/\u2212 mice is also lower than the expression seen for the same allele in naive and flu-infected B27\/ERAP+\/+ mice. In contrast, surface expression of HLA-B7 was unaffected by the absence of ERAP in B7\/ERAP\u2212\/\u2212 transgenic mice. The B7-restricted NP418\u2013426 CTL response in flu-infected B7\/ERAP\u2212\/\u2212 and B7\/ERAP+\/+ mice was also similar. These results provide, to our knowledge, the first in vivo demonstration of ERAP functionally influencing host immune response in an HLA allele-specific manner. This principle has relevance to diseases such as ankylosing spondylitis, in which HLA-B27 and ERAP jointly contribute to disease predisposition.<\/jats:p>","DOI":"10.4049\/jimmunol.1400343","type":"journal-article","created":{"date-parts":[[2014,5,17]],"date-time":"2014-05-17T08:19:35Z","timestamp":1400314775000},"page":"5520-5528","source":"Crossref","is-referenced-by-count":29,"title":["HLA-B27, but Not HLA-B7, Immunodominance to Influenza Is ERAP Dependent"],"prefix":"10.1093","volume":"192","author":[{"given":"Ali","family":"Akram","sequence":"first","affiliation":[{"name":"Division of Genetics & Development, Toronto Western Research Institute , Toronto, Ontario, M5T-2S8","place":["Canada"]},{"name":"Institute of Medical Sciences, University of Toronto Faculty of Medicine , Toronto, Ontario, M5S 1A8","place":["Canada"]},{"name":"Department of Immunology, University of Toronto , Toronto, Ontario, M5S 1A8","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aifeng","family":"Lin","sequence":"additional","affiliation":[{"name":"Division of Genetics & Development, Toronto Western Research Institute , Toronto, Ontario, M5T-2S8","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Gracey","sequence":"additional","affiliation":[{"name":"Division of Genetics & Development, Toronto Western Research Institute , Toronto, Ontario, M5T-2S8","place":["Canada"]},{"name":"Institute of Medical Sciences, University of Toronto Faculty of Medicine , Toronto, Ontario, M5S 1A8","place":["Canada"]},{"name":"Department of Immunology, University of Toronto , Toronto, Ontario, M5S 1A8","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine J","family":"Streutker","sequence":"additional","affiliation":[{"name":"University of Toronto, Department of Laboratory Medicine and Pathobiology. Division of Pathology, St. Michael\u2019s Hospital , Toronto, Ontario, M5B 1W8","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert D","family":"Inman","sequence":"additional","affiliation":[{"name":"Division of Genetics & Development, Toronto Western Research Institute , Toronto, Ontario, M5T-2S8","place":["Canada"]},{"name":"Institute of Medical Sciences, University of Toronto Faculty of Medicine , Toronto, Ontario, M5S 1A8","place":["Canada"]},{"name":"Department of Immunology, University of Toronto , Toronto, Ontario, M5S 1A8","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,6,15]]},"reference":[{"key":"2025032404344830200_r1","doi-asserted-by":"crossref","first-page":"99","DOI":"10.1016\/j.clim.2012.01.015","article-title":"Immunodominance: a pivotal principle in host response to viral infections","volume":"143","author":"Akram","year":"2012","journal-title":"Clin. 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