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

J Kim, JS Kim, HK Lee, HS Kim, EJ Park… - International …, 2018 - Elsevier
J Kim, JS Kim, HK Lee, HS Kim, EJ Park, JE Choi, YJ Choi, BR Shin, EY Kim, JT Hong…
International immunopharmacology, 2018Elsevier
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 …
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.
Elsevier