Tumor inhibition or tumor promotion? The duplicity of CXCR3 in cancer

Tumor tissue includes cancer cells and normal stromal cells such as vascular endothelial cells, connective tissue cells (cancer associated fibroblast, mesenchymal stem cell), and immune cells (tumor‐infiltrating lymphocytes or TIL, dendritic cells, eosinophils, basophils, mast cells, tumor‐associate...

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Veröffentlicht in:Journal of leukocyte biology Jg. 108; H. 2; S. 673 - 685
Hauptverfasser: Russo, Eleonora, Santoni, Angela, Bernardini, Giovanni
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Oxford University Press 01.08.2020
Schlagworte:
Animals
anti‐tumor immunity
Biomarkers
Cancer
cancer immunotherapy
CD8 antigen
Cell activation
Cell survival
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Chemokines
Connective tissues
CXCL10
CXCL10 protein
CXCL11 protein
CXCR3 protein
Dendritic cells
Disease Susceptibility
Endothelial cells
Eosinophils
Gene Duplication
Gene Expression Regulation, Neoplastic
Homeostasis
Humans
Immune response
immune suppression
Immune system
Immunomodulation
Immunotherapy
Inflammation
Leukocytes (basophilic)
Leukocytes (eosinophilic)
Ligands
lymphocyte migration
Lymphocytes
Lymphocytes T
Macrophages
Mast cells
Mesenchymal stem cells
Metastases
Molecular modelling
Natural killer cells
Neoplasms - etiology
Neoplasms - metabolism
Neoplasms - pathology
Protein Binding
Receptors, CXCR3 - genetics
Receptors, CXCR3 - metabolism
Signal Transduction
Solid tumors
Stem cells
Stromal cells
Tumors
CXCL10
anti-tumor immunity
chemokines
immune suppression
cancer immunotherapy
lymphocyte migration
ISSN:0741-5400, 1938-3673, 1938-3673
Online-Zugang:Volltext
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Zusammenfassung:Tumor tissue includes cancer cells and normal stromal cells such as vascular endothelial cells, connective tissue cells (cancer associated fibroblast, mesenchymal stem cell), and immune cells (tumor‐infiltrating lymphocytes or TIL, dendritic cells, eosinophils, basophils, mast cells, tumor‐associated macrophages or TAM, myeloid‐derived suppressor cells or MDSC). Anti‐tumor activity is mainly mediated by infiltration of NK cells, Th1 and CD8+ T cells, and correlates with expression of NK cell and T cell attracting chemokines. Nevertheless, cancer cells hijack tissue homeostasis through secretion of cytokines and chemokines that mediate not only the induction of an inflamed status that supports cancer cell survival and growth, but also the recruitment and/or activation of immune suppressive cells. CXCL9, CXCL10, and CXCL11 are known for their tumor‐inhibiting properties, but their overexpression in several hematologic and solid tumors correlates with disease severity, suggesting a role in tumor promotion. The dichotomous nature of CXCR3 ligands activity mainly depends on several molecular mechanisms induced by cancer cells themselves able to divert immune responses and to alter the whole local environment. A deep understanding of the nature of such phenomenon may provide a rationale to build up a CXCR3/ligand axis targeting strategy. In this review, we will discuss the role of CXCR3 in cancer progression and in regulation of anti‐tumor immune response and immunotherapy. Review on how CXCR3 ligands can shape anti‐tumor immune responses and tumor growth and of the promising possibility to target these molecules for cancer immunotherapy.
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ISSN:0741-5400
1938-3673
1938-3673
DOI:10.1002/JLB.5MR0320-205R