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Int Immunopharmacol. 2018 Oct;63:66-73. doi: 10.1016/j.intimp.2018.07.026. Epub 2018 Jul 31.

CXCR3-deficient natural killer cells fail to migrate to B16F10 melanoma cells.

Author information

1
College of Pharmacy, Chungbuk National University, Cheongju, Chungbuk 28160, Republic of Korea.
2
College of Pharmacy, Chungbuk National University, Cheongju, Chungbuk 28160, Republic of Korea. Electronic address: shan@chungbuk.ac.kr.

Abstract

Natural killer (NK) cells eliminate cancer cells in a contact-dependent manner. However, how NK cells find cancer cells remain unclear. Here, using time-lapse imaging, we investigated how individual NK cells migrate toward cancer cells. Although naïve B16F10 cancer cells produce low levels of chemokines, IFN-γ-treated B16F10 cells secreted high levels of CXCL10, low levels of CCL5, but did not secrete CCL2, CCL7, or CXCL12. Wild-type NK cells migrated well toward cancer cells and killed them, whereas NK cells deficient in CXCR3 did not. CXCR3-deficient NK cells also showed slower migration speed than did wild-type NK cells. Taken together, our data show that NK cells find cancer cells, at least in part, by sensing CXCL10 produced by cancer cells and suggest that a strategy to increase CXCL10 secretion by cancer cells may improve the efficacy of NK cell-based immunotherapy.

KEYWORDS:

CXCL10–CXCR3 axis; Migration; Natural killer cells

PMID:
30075430
DOI:
10.1016/j.intimp.2018.07.026
[Indexed for MEDLINE]

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