The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
cDC1 prime and are licensed by CD4(+) T cells to induce anti-tumour immunity
Open accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“cDC1 are critical for antigen cross-presentation required to prime CD8+ T cells for optimal anti-tumor immunity and priming of CD4+ T cells at early stages, partly because cDC1 provides antigen transportation to lymph nodes for processing by cDC2 (36).”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [36]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“CD40 signaling in cDC1 is required for tumor rejection by playing a key role in augmenting the proliferation of antigen-specific CD8+ T cells (36).”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [36]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Cre reporter strains produced by targeted insertion of EYFP and ECFP into the ROSA26 locus
Srinivas, S., Watanabe, T., Lin, C.-S., William, C. M., Tanabe, Y., Jessell, T. M., & Costantini, F. (2001) · BMC Developmental Biology · doi:10.1186/1471-213x-1-4 · Cited by 3,121
T-cell help for cytotoxic T lymphocytes is mediated by CD40–CD40L interactions
Schoenberger, S. P., Toes, R. E. M., van der Voort, E. I. H., Offringa, R., & Melief, C. J. M. (1998) · Nature · doi:10.1038/31002 · Cited by 2,615
A conditioned dendritic cell can be a temporal bridge between a CD4+ T-helper and a T-killer cell
Ridge, J. P., Rosa, F. D., & Matzinger, P. (1998) · Nature · doi:10.1038/30989 · Cited by 2,360
Help for cytotoxic-T-cell responses is mediated by CD40 signalling
Bennett, S. R. M., Carbone, F., Karamalis, F., Flavell, R. A., Miller, J. F. A. P., & Heath, W. R. (1998) · Nature · doi:10.1038/30996 · Cited by 2,091
Batf3 Deficiency Reveals a Critical Role for CD8α + Dendritic Cells in Cytotoxic T Cell Immunity
Hildner, K., Edelson, B. T., Purtha, W. E., Diamond, M., Matsushita, H., Kohyama, M., Calderon, B., Schraml, B. U., Unanue, E. R., Diamond, M. S., et al. (2008) · Science · doi:10.1126/science.1164206 · Cited by 2,081
Dendritic cells, monocytes and macrophages: a unified nomenclature based on ontogeny
Guilliams, M., Ginhoux, F., Jakubzick, C., Naik, S. H., Onai, N., Schraml, B. U., Segura, É., Tussiwand, R., & Yona, S. (2014) · Nature reviews. Immunology · doi:10.1038/nri3712 · Cited by 1,923
CD4+ T cell help in cancer immunology and immunotherapy
Borst, J., Ahrends, T., Bąbała, N., Melief, C. J. M., & Kastenmüller, W. (2018) · Nature Reviews Immunology · doi:10.1038/s41577-018-0044-0 · Cited by 1,585
Differential Antigen Processing by Dendritic Cell Subsets in Vivo
Dudziak, D., Kamphorst, A. O., Heidkamp, G. F., Buchholz, V. R., Trumpfheller, C., Yamazaki, S., Cheong, C., Liu, K., Lee, H., Park, C. G., et al. (2007) · Science · doi:10.1126/science.1136080 · Cited by 1,454
Cancer exome analysis reveals a T-cell-dependent mechanism of cancer immunoediting
Matsushita, H., Vesely, M. D., Koboldt, D. C., Rickert, C. G., Uppaluri, R., Magrini, V. J., Arthur, C. D., White, J. M., Chen, Y.-S., Shea, L. K., et al. (2012) · Nature · doi:10.1038/nature10755 · Cited by 1,285
Defective CD8 T Cell Memory Following Acute Infection Without CD4 T Cell Help
Sun, J. C., & Bevan, M. J. (2003) · Science · doi:10.1126/science.1083317 · Cited by 1,213
Cited by
Sorted by citations
Items 601–615 of 615
Jia, C., Li, S., Chen, M., Yang, W., Song, Y., Wang, A., & Liu, B. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1963773
Erythropoietin impacts immune adaptation through myeloid-cell programming
Zhang, X., & Engleman, E. G. (2026) · Trends in Immunology · doi:10.1016/j.it.2026.08.014
Li, X., Meng, Y., Dong, J., Ma, Y., Liu, D., Zhang, X., & Zhao, L. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1941235
A matrikine organizes the dendritic cell–T cell triads that build tertiary lymphoid structuresPreprint
Lagal, D. J., Hong, D., Papadas, A., Yacu, G., Geatches, E., Leschinsky, N., Huang, Y., Dou, Y., Fields, M., Gibbons, A., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.09.24.753585
Prognostic value of T lymphocyte CD40L expression levels in patients with sepsis
Shao, B., Huang, Z., Liu, Y., Wang, Z., Huang, F., & Wang, J. (2026) · Frontiers in Medicine · doi:10.3389/fmed.2026.1949041
Yin, J., Lu, S., Liu, Y., Gong, M., Zha, Y., & Jiang, X. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1928701
Li, X., Qiao, L., Wang, W., Xiong, Y., Zhang, L., Shan, G., Sun, Q., Ding, T., & He, X. (2026) · ACS Nano · doi:10.1021/acsnano.6c11994
Gan, L., Liu, Z., Cao, L., Meng, X., Liu, X., Wang, X., & He, Y. (2026) · Experimental Hematology and Oncology · doi:10.1186/s40164-026-00837-6
毕妍娜, Zhao, Y., Ge, Y., 陳, 哲., Zhao, L., & Sun, G. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218859
Senescence and tumor immunology: A multifaceted interplay of influence
Xie, Y., Zhang, J., Wang, S., Rao, D., Zhang, J., & Ao, Y. (2026) · iScience · doi:10.1016/j.isci.2026.117849
Turning cold tumors hot: Strategies to enhance antitumor immunity
Steffensen, V. G., Bratina, M., Tsiavou, C., Schmiegelow, K., & Zio, D. D. (2026) · The Journal of Experimental Medicine · doi:10.1084/jem.20260378
Ge, L., Wang, D., & Tang, B. Z. (2026) · Journal of Controlled Release · doi:10.1016/j.jconrel.2026.115462
Engineered nanobiotechnology for cancer immunotherapy
Mao, C., Liu, Y., & Wang, J. (2026) · 中国科学通报：英文版 · doi:10.1016/j.scib.2026.10.062
Zanotta, S., & Galati, D. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27219607
Luri‐Rey, C., Rodríguez, I., Arrieta-Aranzueque, S., Guillamón, D. R., Vercher, E., Soria, N., Molero-Glez, P., Cuesta, R., Gomis, G., Azpilikueta, A., et al. (2026) · Immunity · doi:10.1016/j.immuni.2026.10.003
Metadata
- 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
- Venue
- Nature
- Published
- 2020-08-12
- Volume
- 584
- Issue
- 7822
- Pages
- 624-629
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- 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
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
