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Cancer Immunology Research
Cancer Immunology Research

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Research Articles

Batf3-Dependent Genes Control Tumor Rejection Induced by Dendritic Cells Independently of Cross-Presentation

Derek J. Theisen, Stephen T. Ferris, Carlos G. Briseño, Nicole Kretzer, Arifumi Iwata, Kenneth M. Murphy and Theresa L. Murphy
Derek J. Theisen
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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  • ORCID record for Derek J. Theisen
Stephen T. Ferris
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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Carlos G. Briseño
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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Nicole Kretzer
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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Arifumi Iwata
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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Kenneth M. Murphy
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.Howard Hughes Medical Institute, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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Theresa L. Murphy
Department of Pathology and Immunology, Washington University in St. Louis, School of Medicine, St. Louis, Missouri.
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  • ORCID record for Theresa L. Murphy
  • For correspondence: tmurphy@wustl.edu
DOI: 10.1158/2326-6066.CIR-18-0138 Published January 2019
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Abstract

The BATF3-dependent cDC1 lineage of conventional dendritic cells (cDC) is required for rejection of immunogenic sarcomas and for rejection of progressive sarcomas during checkpoint blockade therapy. One unique function of the cDC1 lineage is the efficient cross-presentation of tumor-derived neoantigens to CD8+ T cells, but it is not clear that this is the only unique function of cDC1 required for tumor rejection. We previously showed that BATF3 functions during cDC1 lineage commitment to maintain IRF8 expression in the specified cDC1 progenitor. However, since cDC1 progenitors do not develop into mature cDC1s in Batf3−/− mice, it is still unclear whether BATF3 has additional functions in mature cDC1 cells. A transgenic Irf8-Venus reporter allele increases IRF8 protein concentration sufficiently to allow autonomous cDC1 development in spleens of Batf3−/− mice. These restored Batf3−/− cDC1s are transcriptionally similar to control wild-type cDC1s but have reduced expression of a restricted set of cDC1-specific genes. Restored Batf3−/− cDC1s are able to cross-present cell-associated antigens both in vitro and in vivo. However, Batf3−/− cDC1 exhibit altered characteristics in vivo and are unable to mediate tumor rejection. These results show that BATF3, in addition to regulating Irf8 expression to stabilize cDC1 lineage commitment, also controls expression of a small set of genes required for cDC1-mediated tumor rejection. These BATF3-regulated genes may be useful targets in immunotherapies aimed at promoting tumor rejection.

Footnotes

  • Note: Supplementary data for this article are available at Cancer Immunology Research Online (http://cancerimmunolres.aacrjournals.org/).

  • Received March 5, 2018.
  • Revision received September 12, 2018.
  • Accepted November 21, 2018.
  • Published first November 27, 2018.
  • ©2018 American Association for Cancer Research.
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Cancer Immunology Research: 7 (1)
January 2019
Volume 7, Issue 1
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Batf3-Dependent Genes Control Tumor Rejection Induced by Dendritic Cells Independently of Cross-Presentation
Derek J. Theisen, Stephen T. Ferris, Carlos G. Briseño, Nicole Kretzer, Arifumi Iwata, Kenneth M. Murphy and Theresa L. Murphy
Cancer Immunol Res January 1 2019 (7) (1) 29-39; DOI: 10.1158/2326-6066.CIR-18-0138

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Batf3-Dependent Genes Control Tumor Rejection Induced by Dendritic Cells Independently of Cross-Presentation
Derek J. Theisen, Stephen T. Ferris, Carlos G. Briseño, Nicole Kretzer, Arifumi Iwata, Kenneth M. Murphy and Theresa L. Murphy
Cancer Immunol Res January 1 2019 (7) (1) 29-39; DOI: 10.1158/2326-6066.CIR-18-0138
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