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

Tokunaga, Ryuma; Zhang, Wu; Naseem, Madiha; Puccini, Alberto; Berger, Martin Dave; Soni, Shivani; McSkane, Michelle; Baba, Hideo; Lenz, Heinz-Josef (2018). CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - A target for novel cancer therapy. Cancer treatment reviews, 63, pp. 40-47. Elsevier 10.1016/j.ctrv.2017.11.007

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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.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Medical Oncology

UniBE Contributor:

Berger, Martin Dave

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1532-1967

Publisher:

Elsevier

Language:

English

Submitter:

Nicole Corminboeuf

Date Deposited:

16 Apr 2018 14:35

Last Modified:

03 Nov 2019 09:10

Publisher DOI:

10.1016/j.ctrv.2017.11.007

PubMed ID:

29207310

Uncontrolled Keywords:

CXCL10 CXCL11 CXCL9 CXCR3 Cancer Immunotherapy

BORIS DOI:

10.7892/boris.111356

URI:

https://boris.unibe.ch/id/eprint/111356

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