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dc.contributor.authorBanach, Maureen
dc.contributor.authorEdholm, Eva-Stina Isabella
dc.contributor.authorGonzalez, Xavier
dc.contributor.authorBenraiss, Abdellatif
dc.contributor.authorRobert, Jaques
dc.date.accessioned2020-02-04T12:42:52Z
dc.date.available2020-02-04T12:42:52Z
dc.date.issued2019-06-01
dc.description.abstractThe conditions that lead to antitumor or protumor functions of natural killer T (NKT) cells against mammalian tumors are only partially understood. Therefore, insights into the evolutionary conservation of NKT and their analogs—innate-like T (iT) cells—may reveal factors that contribute to tumor eradication. As such, we investigated the amphibian <i>Xenopus laevis</i> iT cells and interacting MHC class I-like (<i>XNC</i> or <i>mhc1b.L</i>) genes against ff-2 thymic lymphoid tumors. Upon ff-2 intraperitoneal transplantation into syngeneic tadpoles, two iT cell subsets iVα6 and iVα22, characterized by an invariant T-cell receptor α chain rearrangement (Vα6-Jα1.43 and Vα22-Jα1.32 respectively), were recruited to the peritoneum, concomitant with a decreased level of these transcripts in the spleen and thymus. To address the hypothesize that different iT cell subsets have distinct, possibly opposing, roles upon ff-2 tumor challenge, we determined whether ff-2 tumor growth could be manipulated by impairing Vα6 iT cells or by deleting their restricting element, the <i>XNC</i> gene, <i>XNC10</i> (<i>mhc1b10.1.L</i>), on ff-2 tumors. Accordingly, the <i>in vivo</i> depletion of Vα6 iT cells using XNC10-tetramers enhanced tumor growth, indicating Vα6 iT cell-mediated antitumor activities. However, <i>XNC10</i>-deficient transgenic tadpoles that also lack Vα6 iT cells were resistant to ff-2 tumors, uncovering a potential new function of <i>XNC10</i> besides Vα6 iT cell development. Furthermore, the CRISPR/Cas9-mediated knockout of <i>XNC10</i> in ff-2 tumors broke the immune tolerance. Together, our findings demonstrate the relevance of XNC10/iT cell axis in controlling <i>Xenopus</i> tumor tolerance or rejection.en_US
dc.descriptionThis is a pre-copyedited, author-produced version of an article accepted for publication in Carcinogenesis following peer review. The version of record Banach, M., Edholm, E.-S., Gonzalez, X., Benraiss, A. & Robert, J. (2019). Impacts of the MHC class I-like XNC10 and innate-like T cells on tumor tolerance and rejection in the amphibian Xenopus. <i>Carcinogenesis, 40</i>(7), 924–935. is available online at: <a href=https://doi.org/10.1093/carcin/bgz100>https://doi.org/10.1093/carcin/bgz100</a>en_US
dc.identifier.citationBanach, Edholm ES, Gonzalez, Benraiss, Robert. Impacts of the MHC class I-like XNC10 and innate-like T cells on tumor tolerance and rejection in the amphibian Xenopus.. Carcinogenesis. 2019;40(7):924-935en_US
dc.identifier.cristinIDFRIDAID 1773509
dc.identifier.doihttps://doi.org/10.1093/carcin/bgz100
dc.identifier.issn0143-3334
dc.identifier.urihttps://hdl.handle.net/10037/17321
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.relation.journalCarcinogenesis
dc.rights.accessRightsopenAccessen_US
dc.rights.holder© The Author(s) 2019. Published by Oxford University Press. All rights reserved.en_US
dc.subjectVDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710en_US
dc.subjectVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710en_US
dc.titleImpacts of the MHC class I-like XNC10 and innate-like T cells on tumor tolerance and rejection in the amphibian Xenopusen_US
dc.type.versionacceptedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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