Mini Review ARTICLE
The role of CXC chemokine receptors 1-4 on immune cells in the tumor microenvironment
- 1Medicine, Huddinge, Karolinska Institutet (KI), Sweden
- 2Cell Therapy Institute, Nova Southeastern University, United States
- 3Oncology-Pathology, Karolinska Institutet (KI), Sweden
Chemokines govern leukocyte migration by attracting cells that express their cognate ligands. Many cancer types show altered chemokine secretion profiles, favouring the recruitment of pro-tumorigenic immune cells and preventing the accumulation of anti-tumorigenic effector cells. This can ultimately results in cancer immune evasion. The manipulation of chemokine and chemokine-receptor signalling can reshape the immunological phenotypes within the tumor microenvironment in order to increase the therapeutic efficacy of cancer immunotherapy. Here we discuss the three chemokine-chemokine receptor axes, CXCR1/2–CXCL1-3/5-8, CXCR3–CXCL9/10/11, and CXCR4-CXCL12 and their role on pro-tumorigenic immune cells and anti-tumorigenic effector cells in solid tumors. In particular, we summarize current strategies to target these axes and discuss their potential use in treatment approaches.
Keywords: Chemokines, cancer immunotherapy, metastasis, NK cells, T cells, Myeloid Cells
Received: 29 May 2018;
Accepted: 31 Aug 2018.
Edited by:Giovanni Bernardini, Università degli Studi di Roma La Sapienza, Italy
Reviewed by:Paul Proost, Rega Institute for Medical Research, KU Leuven, Belgium
Roberta Castriconi, Dipartimento di Medicina Sperimentale, Università degli studi di Genova, Italy
Copyright: © 2018 Susek, Karvouni, Alici and Lundqvist. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: PhD. Andreas Lundqvist, Karolinska Institutet (KI), Oncology-Pathology, Solna, Sweden, Andreas.Lundqvist@ki.se