Tumor-reactive CD4(+) T cells develop cytotoxic activity and eradicate large established melanoma after transfer into lymphopenic hosts
Open accessAbstract
Adoptive transfer of large numbers of tumor-reactive CD8(+) cytotoxic T lymphocytes (CTLs) expanded and differentiated in vitro has shown promising clinical activity against cancer. However, such protocols are complicated by extensive ex vivo manipulations of tumor-reactive cells and have largely focused on CD8(+) CTLs, with much less emphasis on the role and contribution of CD4(+) T cells. Using a mouse model of advanced melanoma, we found that transfer of small numbers of naive tumor-reactive CD4(+) T cells into lymphopenic recipients induces substantial T cell expansion, differentiation, and regression of large established tumors without the need for in vitro manipulation. Surprisingly, CD4(+) T cells developed cytotoxic activity, and tumor rejection was dependent on class II-restricted recognition of tumors by tumor-reactive CD4(+) T cells. Furthermore, blockade of the coinhibitory receptor CTL-associated antigen 4 (CTLA-4) on the transferred CD4(+) T cells resulted in greater expansion of effector T cells, diminished accumulation of tumor-reactive regulatory T cells, and superior antitumor activity capable of inducing regression of spontaneous mouse melanoma. These findings suggest a novel potential therapeutic role for cytotoxic CD4(+) T cells and CTLA-4 blockade in cancer immunotherapy, and demonstrate the potential advantages of differentiating tumor-reactive CD4(+) cells in vivo over current protocols favoring in vitro expansion and differentiation.
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Tumor regression was dependent on class II-restricted recognition of tumors by tumor-reactive CD4+ CTLs which developed cytotoxic activity and kill tumor.
“Tumor regression was dependent on class II-restricted recognition of tumors by tumor-reactive CD4+ CTLs which developed cytotoxic activity and kill tumor (54).”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [54]
CD4+ T cells also contribute to direct tumor killing besides their supporting role as cytokine producers.
“Although CD8+ T cells are known to play a pivotal role in antitumor immunity, CD4+ T cells also contribute to direct tumor killing besides their supporting role as cytokine producers.”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [54]
Upon transferring of naive tumor reactive CD4+ T cells into lymphopenic recipients, substantial T cell expansion and differentiation were observed.
“Upon transferring of naive tumor reactive CD4+ T cells into lymphopenic recipients, substantial T cell expansion and differentiation were observed.”
From mRNA vaccine with unmodified uridine induces robust type I interferon-dependent anti-tumor immunity in a melanoma model (2022) · cites this paper as [54]
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- Authors
- Quezada, S. A., Simpson, T. R., Peggs, K. S., Merghoub, T., Vider, J., Fan, X., Blasberg, R., Yagita, H., Muranski, P., Antony, P. A., Restifo, N. P., & Allison, J. P.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Department of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan 4
- National Institutes of Health (US)
- University of Maryland, Baltimore (US)
- Corresponding author
- Allison, James P.
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2010-02-15
- Volume
- 207
- Issue
- 3
- Pages
- 637-650
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2839156
- OpenAlex
- W2053967595
- Cited by
- 898
- References
- 50
- Citations by year
- 2026: 41 · 2025: 58 · 2024: 45 · 2023: 58 · 2022: 62 · 2021: 93 · 2020: 65 · 2019: 53 · 2018: 50 · 2017: 52 · 2016: 54 · 2015: 56 · 2014: 48 · 2013: 48 · 2012: 53
- FWCI
- 22.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Griffith Research Online (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Cancer Research Institute
- Memorial Sloan-Kettering Cancer Center
- Swim Across America
- University College London
- Canadian Institutes of Health Research
- Japan Society for the Promotion of Science (22240089)
- 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
- CD4+ T cells, melanoma, adoptive T cell therapy, cytotoxic T lymphocytes, CTLA-4 blockade, lymphopenia, tumor rejection, regulatory T cells, cancer immunotherapy, spontaneous tumor regression
- MeSH terms
- Animals, Cell Differentiation, Cell Division, Disease Models, Animal, Interferon-gamma, Melanoma, Melanoma, Experimental, Mice, Transgenic, T-Lymphocytes, Cytotoxic, Trypsin, Leukemia, T-Cell, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, 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 ›
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