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Cancer Immunology Research
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Research Article

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
1Washington University School of Medicine
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Stephen T Ferris
2Department of Pathology and Immunology, Washington University School of Medicine
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Carlos G Briseño
3Amgen Inc
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Nicole Kretzer
4Obstetrics and Gynecology, University of Washington
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Arifumi Iwata
5Department of Allergy and Clinical Immunology, Chiba University Hospital
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Kenneth M. Murphy
2Department of Pathology and Immunology, Washington University School of Medicine
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Theresa L Murphy
6Pathology and Immunology, Washington University School of Medicine
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  • For correspondence: tmurphy@wustl.edu
DOI: 10.1158/2326-6066.CIR-18-0138
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Abstract

The BATF3-dependent cDC1 lineage of conventional dendritic cells (cDCs) 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.

  • Received March 5, 2018.
  • Revision received September 12, 2018.
  • Accepted November 21, 2018.
  • Copyright ©2018, American Association for Cancer Research.
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This OnlineFirst version was published on November 27, 2018
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 November 27 2018 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 November 27 2018 DOI: 10.1158/2326-6066.CIR-18-0138
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Cancer Immunology Research
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