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dc.contributor.authorWhyte, C.E.-
dc.contributor.authorOsman, M.-
dc.contributor.authorKara, E.E.-
dc.contributor.authorAbbott, C.-
dc.contributor.authorFoeng, J.-
dc.contributor.authorMcKenzie, D.R.-
dc.contributor.authorFenix, K.A.-
dc.contributor.authorHarata-Lee, Y.-
dc.contributor.authorFoyle, K.L.-
dc.contributor.authorBoyle, S.T.-
dc.contributor.authorKochetkova, M.-
dc.contributor.authorAguilera, A.R.-
dc.contributor.authorHou, J.-
dc.contributor.authorLi, X.-Y.-
dc.contributor.authorArmstrong, M.A.-
dc.contributor.authorPederson, S.M.-
dc.contributor.authorComerford, I.-
dc.contributor.authorSmyth, M.J.-
dc.contributor.authorMcColl, S.R.-
dc.identifier.citationJournal of Experimental Medicine, 2020; 217(6):1-S4-
dc.description.abstractCurrent immunotherapies involving CD8⁺ T cell responses show remarkable promise, but their efficacy in many solid tumors is limited, in part due to the low frequency of tumor-specific T cells in the tumor microenvironment (TME). Here, we identified a role for host atypical chemokine receptor 4 (ACKR4) in controlling intratumor T cell accumulation and activation. In the absence of ACKR4, an increase in intratumor CD8⁺ T cells inhibited tumor growth, and nonhematopoietic ACKR4 expression was critical. We show that ACKR4 inhibited CD103⁺ dendritic cell retention in tumors through regulation of the intratumor abundance of CCL21. In addition, preclinical studies indicate that ACKR4 and CCL21 are potential therapeutic targets to enhance responsiveness to immune checkpoint blockade or T cell costimulation.-
dc.description.statementofresponsibilityCarly E. Whyte, Maleika Osman, Ervin E. Kara, Caitlin Abbott, Jade Foeng, Duncan R. McKenzie, Kevin A. Fenix, Yuka Harata-Lee, Kerrie L. Foyle, Sarah T. Boyle, Marina Kochetkova, Amelia Roman Aguilera, Jiajie Hou, Xian-Yang Li, Mark A. Armstrong, Stephen M. Pederson, Iain Comerford, Mark J. Smyth, and Shaun R. McColl-
dc.publisherRockefeller University Press-
dc.rights© 2020 Crown copyright. The government of Australia, Canada, or the UK ("the Crown") owns the copyright interests of authors who are government employees. The Crown Copyright is not transferable. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at
dc.subjectDendritic Cells-
dc.subjectCD8-Positive T-Lymphocytes-
dc.subjectStromal Cells-
dc.subjectMice, Inbred C57BL-
dc.subjectNeoplasm Metastasis-
dc.subjectDisease Models, Animal-
dc.subjectIntegrin alpha Chains-
dc.subjectAntigens, CD-
dc.subjectSurvival Analysis-
dc.subjectCell Proliferation-
dc.subjectReceptors, CCR-
dc.subjectChemokine CCL21-
dc.subjectImmune Checkpoint Inhibitors-
dc.titleACKR4 restrains antitumor immunity by regulating CCL21-
dc.typeJournal article-
dc.identifier.orcidAbbott, C. [0000-0002-1024-1524]-
dc.identifier.orcidFenix, K.A. [0000-0003-1619-1406]-
dc.identifier.orcidFoyle, K.L. [0000-0002-2663-4621]-
dc.identifier.orcidPederson, S.M. [0000-0001-8197-3303]-
dc.identifier.orcidMcColl, S.R. [0000-0003-0949-4660]-
Appears in Collections:Aurora harvest 4
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