CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - a target for novel cancer therapy

Tokunaga, Ryuma; Zhang, Wu; Naseem, Madiha; Puccini, Alberto; Berger, Martin D; Soni, Shivani; McSkane, Michelle; Baba, Hideo; Lenz, Heinz-Josef

doi:10.1016/j.ctrv.2017.11.007

Cited by 1,627Chemokine receptors and signalingCancer Immunotherapy and BiomarkersConnective Tissue Growth Factor Research

CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - a target for novel cancer therapy

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Tokunaga, Ryuma, Zhang, Wu, Naseem, Madiha, Puccini, Alberto, Berger, Martin D, Soni, Shivani, McSkane, Michelle, Baba, Hideo +1 more·2018·Cancer Treatment Reviews

DOI 10.1016/j.ctrv.2017.11.007PMC PMC5801162

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Abstract

Chemokines are proteins which induce chemotaxis, promote differentiation of immune cells, and cause tissue extravasation. Given these properties, their role in anti-tumor immune response in the cancer environment is of great interest. Although immunotherapy has shown clinical benefit for some cancer patients, other patients do not respond. One of the mechanisms of resistance to checkpoint inhibitors may be chemokine signaling. The CXCL9, -10, -11/CXCR3 axis regulates immune cell migration, differentiation, and activation, leading to tumor suppression (paracrine axis). However, there are some reports that show involvements of this axis in tumor growth and metastasis (autocrine axis). Thus, a better understanding of CXCL9, -10, -11/CXCR3 axis is necessary to develop effective cancer control. In this article, we summarize recent evidence regarding CXCL9, CXCL10, CXCL11/CXCR3 axis in the immune system and discuss their potential role in cancer treatment.

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The CXCL9/10/11-CXCR3 pathway is well known for recruiting and activating cytotoxic T cells.
“The relevance of the CXCL9/10/11-CXCR3 pathway for recruiting and triggering cytotoxic T cells is well known (47-50,64).”
From Exercise Training Improves Tumor Control by Increasing CD8+ T-cell Infiltration via CXCR3 Signaling and Sensitizes Breast Cancer to Immune Checkpoint Blockade (2021) · cites this paper as [48]
CXCL9, CXCL10, and CXCL11 are CXCR3 ligands that promote trafficking of CD8+CXCR3+ T cells into tumors.
“CXCL9/10/11 are ligands of the CXCR3 receptor involved in increased trafficking of CD8+CXCR3+ T cells to tumors (47,48,64).”
From Exercise Training Improves Tumor Control by Increasing CD8+ T-cell Infiltration via CXCR3 Signaling and Sensitizes Breast Cancer to Immune Checkpoint Blockade (2021) · cites this paper as [48]
Because CXCL11 is nonfunctional in C57BL/6 mice, it was measured only in the FVB MCa-M3C tumor model.
“CXCL11 is not functional in C57BL/6 mice, so it was only quantified in the MCa-M3C tumor model in FVB mice (48).”
From Exercise Training Improves Tumor Control by Increasing CD8+ T-cell Infiltration via CXCR3 Signaling and Sensitizes Breast Cancer to Immune Checkpoint Blockade (2021) · cites this paper as [48]

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CHEMOKINES, CXC | CXCL9 (MIG)
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Authors: Tokunaga, R., Zhang, W., Naseem, M., Puccini, A., Berger, M. D., Soni, S., McSkane, M., Baba, H., & Lenz, H.-J.
Affiliations: University of Southern California (US)
Kumamoto University (JP)
Corresponding author: Lenz, Heinz-Josef
ORCID: Tokunaga, Ryuma
Naseem, Madiha
Puccini, Alberto
Berger, Martin D
Soni, Shivani
McSkane, Michelle
Baba, Hideo
Lenz, Heinz-Josef
Venue: Cancer Treatment Reviews
Publisher: Elsevier BV
Published: 2018-02
Volume: 63
Pages: 40-47
ISSN: 0305-7372 (ISSN-L)
DOI: 10.1016/j.ctrv.2017.11.007
PMC: PMC5801162
OpenAlex: W2770893462
Cited by: 1,627
References: 99
Citations by year: 2026: 239 · 2025: 253 · 2024: 286 · 2023: 216 · 2022: 226 · 2021: 184 · 2020: 149 · 2019: 58 · 2018: 15
FWCI: 6.37
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (am, 307 d)
Locations: Cancer Treatment Reviews (acceptedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Bern Open Repository and Information System (University of Bern) (submittedVersion)
Funders: National Cancer Institute (R01CA166161, P30CA014089)
Topics: Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
Keywords: CXCL9, CXCL10, CXCL11, CXCR3, chemokines, chemokine signaling, antitumor immunity, leukocyte migration, tumor microenvironment, immune checkpoint inhibitors, immunotherapy resistance, tumor growth, metastasis, autocrine and paracrine signaling, cancer immunotherapy targets
MeSH terms: Animals, Humans, Lymphocyte Activation, Neoplasms, Chemokine CXCL10, Receptors, CXCR3, Chemokine CXCL9, Chemokine CXCL11

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CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - a target for novel cancer therapy

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