Cited by 615Immunotherapy and Immune ResponsesT-cell and B-cell ImmunologyCancer Immunotherapy and Biomarkers

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cDC1 prime and are licensed by CD4(+) T cells to induce anti-tumour immunity

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Ferris, Stephen T., Durai, Vivek, Wu, Renee, Theisen, Derek J., Ward, Jeffrey P., Bern, Michael D., Davidson, Jesse T., Bagadia, Prachi, Liu, Tiantian, Briseño, Carlos G., Li, Lijin, Gillanders, William E., Wu, Gregory F., Yokoyama, Wayne M., Murphy, Theresa L., Schreiber, Robert D., Murphy, Kenneth M.·2020·Nature

DOI 10.1038/s41586-020-2611-3PMC PMC7469755

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Abstract

Conventional type 1 dendritic cells (cDC1)1 are thought to perform antigen cross-presentation, which is required to prime CD8+ T cells 2,3, whereas cDC2 are specialized for priming CD4+ T cells 4,5. CD4+ T cells are also considered to help CD8+ T cell responses through a variety of mechanisms 6-11, including a process whereby CD4+ T cells 'license' cDC1 for CD8+ T cell priming 12. However, this model has not been directly tested in vivo or in the setting of help-dependent tumour rejection. Here we generated an Xcr1 Cre mouse strain to evaluate the cellular interactions that mediate tumour rejection in a model requiring CD4+ and CD8+ T cells. As expected, tumour rejection required cDC1 and CD8+ T cell priming required the expression of major histocompatibility class I molecules by cDC1. Unexpectedly, early priming of CD4+ T cells against tumour-derived antigens also required cDC1, and this was not simply because they transport antigens to lymph nodes for processing by cDC2, as selective deletion of major histocompatibility class II molecules in cDC1 also prevented early CD4+ T cell priming. Furthermore, deletion of either major histocompatibility class II or CD40 in cDC1 impaired tumour rejection, consistent with a role for cognate CD4+ T cell interactions and CD40 signalling in cDC1 licensing. Finally, CD40 signalling in cDC1 was critical not only for CD8+ T cell priming, but also for initial CD4+ T cell activation. Thus, in the setting of tumour-derived antigens, cDC1 function as an autonomous platform capable of antigen processing and priming for both CD4+ and CD8+ T cells and of the direct orchestration of their cross-talk that is required for optimal anti-tumour immunity.

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Authors: Ferris, S. T., Durai, V., Wu, R., Theisen, D. J., Ward, J. P., Bern, M. D., Davidson, J. T., Bagadia, P., Liu, T., Briseño, C. G., Li, L., Gillanders, W. E., Wu, G. F., Yokoyama, W. M., Murphy, T. L., Schreiber, R. D., & Murphy, K. M.
Affiliations: Washington University in St. Louis (US)
University of California, San Francisco (US)
Barnes-Jewish Hospital (US)
Howard Hughes Medical Institute (US)
Corresponding author: Murphy, Kenneth M.
ORCID: Ferris, Stephen T.
Durai, Vivek
Wu, Renee
Theisen, Derek J.
Ward, Jeffrey P.
Bern, Michael D.
Davidson, Jesse T.
Bagadia, Prachi
Liu, Tiantian
Briseño, Carlos G.
Li, Lijin
Gillanders, William E.
Wu, Gregory F.
Yokoyama, Wayne M.
Murphy, Theresa L.
Schreiber, Robert D.
Murphy, Kenneth M.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2020-08-12
Volume: 584
Issue: 7822
Pages: 624-629
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/s41586-020-2611-3
PMC: PMC7469755
OpenAlex: W3048641542
Cited by: 611
References: 50
Citations by year: 2026: 112 · 2025: 105 · 2024: 112 · 2023: 127 · 2022: 76 · 2021: 67 · 2020: 12
FWCI: 24.74
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Howard Hughes Medical Institute
National Institutes of Health (UL1TR000448, UL1TR002345)
National Cancer Institute (T32CA009573, R01CA190700, T32CA009621, R01CA248919, P30CA091842)
National Institute of Allergy and Infectious Diseases (R01AI150297, R01AI129545, T32AI007163, R01AI162643)
National Institute of Diabetes and Digestive and Kidney Diseases (F30DK108498, F30DK112466)
National Institute of Neurological Disorders and Stroke (R01NS106289)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR073752)
National Center for Advancing Translational Sciences
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Keywords: conventional type 1 dendritic cells, cDC1, CD4+ T cell priming, CD8+ T cell priming, MHC class II, MHC class I, cross-presentation, tumor rejection, antitumor immunity
MeSH terms: Animals, Histocompatibility Antigens Class II, Dendritic Cells, Female, Neoplasms, Signal Transduction, CD4-Positive T-Lymphocytes, Antigen Presentation, CD8-Positive T-Lymphocytes, CD40 Antigens, Cross-Priming, Mice

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cDC1 prime and are licensed by CD4(+) T cells to induce anti-tumour immunity

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