Non-redundant requirement for CXCR3 signalling during tumoricidal T-cell trafficking across tumour vascular checkpoints
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T-cell trafficking at vascular sites has emerged as a key step in antitumour immunity. Chemokines are credited with guiding the multistep recruitment of CD8+ T cells across tumour vessels. However, the multiplicity of chemokines within tumours has obscured the contributions of individual chemokine receptor/chemokine pairs to this process. Moreover, recent studies have challenged whether T cells require chemokine receptor signalling at effector sites. Here we investigate the hierarchy of chemokine receptor requirements during T-cell trafficking to murine and human melanoma. These studies reveal a non-redundant role for Gαi-coupled CXCR3 in stabilizing intravascular adhesion and extravasation of adoptively transferred CD8+ effectors that is indispensable for therapeutic efficacy. In contrast, functional CCR2 and CCR5 on CD8+ effectors fail to support trafficking despite the presence of intratumoral cognate chemokines. Taken together, these studies identify CXCR3-mediated trafficking at the tumour vascular interface as a critical checkpoint to effective T-cell-based cancer immunotherapy. Tumours secrete many lymphocyte-attracting chemokines. Here the authors show that despite the abundance of their ligands, CCR2 and CCR5 do not mediate trafficking of effector CD8 T cells into the tumour, whereas CXCR3 is essential for this process and for T-cell-based elimination of melanoma in mice.
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CXCL10 and CCL5 are dominant mediators for recruitment of CXCR3+ and CCR5+ tumor-specific T lymphocytes into tumors, and their intratumoral expression correlates with favorable clinical outcomes in melanoma.
“These chemokines have been identified as the dominant mediators for the recruitment of CXCR3+ and CCR5+ tumor-specific T lymphocytes into the tumors and their intratumoral expression correlated with favorable clinical outcomes in patients with melanoma30–32.”
From Epigenetic state determines the in vivo efficacy of STING agonist therapy (2023) · cites this paper as [31]
The Introduction links tumor CXCL9/CXCL10 expression and CCR5 ligands, including CCL5, with T-cell infiltration and favorable clinical outcomes. But the Results identify CXCR3 as required for T-cell entry into melanoma tumors and report that loss of CCR5 did not impair entry. The paper therefore does not support calling CCL5–CCR5 a dominant recruitment pathway alongside CXCL10–CXCR3. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTogether with CXCL9, CXCL10 is a dominant chemokine for the recruitment of tumor-specific CD8+ T cells into tumors.
“Together with CXCL9, another CXCR3-binding chemokine, CXCL10 is a dominant chemokine for the recruitment of tumor-specific CD8+ T cells into the tumors31,32.”
From Epigenetic state determines the in vivo efficacy of STING agonist therapy (2023) · cites this paper as [31]
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- Authors
- Mikucki, M. E., Fisher, D. T., Matsuzaki, J., Skitzki, J. J., Gaulin, N. B., Muhitch, J. B., Ku, A. W., Frelinger, J. G., Odunsi, K., Gajewski, T. F., Luster, A. D., & Evans, S. S.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- University of Rochester Medicine (US)
- University of Chicago (US)
- Harvard University (US)
- Corresponding author
- Evans, S. S.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-06-25
- Volume
- 6
- Issue
- 1
- Pages
- 7458-7458
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4605273
- OpenAlex
- W1019458012
- Cited by
- 512
- References
- 71
- Citations by year
- 2026: 46 · 2025: 45 · 2024: 38 · 2023: 51 · 2022: 64 · 2021: 77 · 2020: 54 · 2019: 50 · 2018: 34 · 2017: 29 · 2016: 21 · 2015: 2
- FWCI
- 12.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Roswell Park Cancer Institute (P50CA159981)
- Dartmouth College
- National Institutes of Health (7f30ca177210-03, 5r01ca069212-18, CA069212, AI082039)
- University at Buffalo
- Cancer Institute, University of Pittsburgh (P50CA159981-01A1)
- Audrey and Theodor Geisel School of Medicine at Dartmouth
- National Cancer Institute (R01-CA069212, R01CA158318, CA-069212, R01CA079765, CA79765, 1F30 CA177210, R01CA127475, F30 CA177210, CA127475, CA158318-01A1, T32CA085183, P50CA159981, P30CA016056)
- National Institute of Allergy and Infectious Diseases (R56AI082039, AI082039, R01AI082039)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- CXCR3, T cell migration, tumor vasculature, melanoma, CD8+ T cells, CCR2, CCR5, extravasation, cancer immunotherapy, chemokines
- MeSH terms
- Animals, Cell Movement, Female, Gene Expression Regulation, Melanoma, Melanoma, Experimental, Mice, Transgenic, Neoplasms, Ovalbumin, Signal Transduction, Mice, Knockout, CD8-Positive T-Lymphocytes, Adoptive Transfer, Receptors, CCR5, Mice, Receptors, CXCR3, Receptors, CCR2
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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