{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T10:07:35Z","timestamp":1775124455331,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,1,19]],"date-time":"2017-01-19T00:00:00Z","timestamp":1484784000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003977","name":"Israel Science Foundation","doi-asserted-by":"publisher","award":["1275\/12"],"award-info":[{"award-number":["1275\/12"]}],"id":[{"id":"10.13039\/501100003977","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001698","name":"Israel Cancer Research Fund","doi-asserted-by":"publisher","award":["13\/726\/RCDA"],"award-info":[{"award-number":["13\/726\/RCDA"]}],"id":[{"id":"10.13039\/100001698","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001558","name":"Concern Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001558","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>We report a new mouse strain with a single point mutation in the type 2 transporter associated with antigen processing (TAP2). This strain randomly arose in one of our C57BL\/6J mouse colonies and was initially discovered because of the lack of CD8<jats:sup>+<\/jats:sup> T cells in the periphery. Following our observation, we subsequently revealed a lack of cell surface MHC\u2010I expression, derived from TAP2 protein deficiency. Our strain, named <jats:italic>eightless<\/jats:italic>, has a C to T substitution in exon 5 resulting in a glutamine to stop codon substitution at position 285 in the TAP2 protein. Interestingly, in addition to the expected lack of CD8<jats:sup>+<\/jats:sup> T cell phenotype, <jats:italic>eightless<\/jats:italic> mice have a diminished number of macrophages in their peritoneum. Moreover, following peritoneal inflammation, elicited <jats:italic>eightless<\/jats:italic> macrophages showed impaired survival both <jats:italic>in\u00a0vivo<\/jats:italic> and <jats:italic>ex\u00a0vivo<\/jats:italic>. Our study describes the first ever TAP2 complete knockout mouse strain and provides a possible explanation for why patients with TAP2 deficiency syndrome present clinical manifestations that would suggest a phagocyte defect rather than a lack of CD8<jats:sup>+<\/jats:sup> T cells.<\/jats:p>","DOI":"10.1111\/imm.12694","type":"journal-article","created":{"date-parts":[[2016,11,18]],"date-time":"2016-11-18T17:46:41Z","timestamp":1479491201000},"page":"432-443","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["A novel spontaneous mutation in the TAP2 gene unravels its role in macrophage survival"],"prefix":"10.1111","volume":"150","author":[{"given":"Antonio","family":"Lapenna","sequence":"first","affiliation":[{"name":"The Lautenberg Centre for Immunology and Cancer Research The Biomedical Research Institute Israel\u2013Canada of the Faculty of Medicine The Hebrew University Hadassah Medical School Jerusalem 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