CXCR3-deficient natural killer cells fail to migrate to B16F10 melanoma cells
| Autor: | Youngsoo Kim, Ju Young Kim, Jin Tae Hong, Ji Sung Kim, Hyung Sook Kim, Yeo Jin Choi, Eun Young Kim, Hong Kyung Lee, Jeong Eun Choi, Sang-Bae Han, Bo Ram Shin, Eun Jae Park |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Chemokine Receptors CXCR3 medicine.medical_treatment Immunology Cell Melanoma Experimental Biology CCL2 CXCR3 CCL5 03 medical and health sciences 0302 clinical medicine Cell Line Tumor medicine Animals Immunology and Allergy CXCL10 Mice Knockout Pharmacology Immunotherapy Chemokine CXCL10 Killer Cells Natural Mice Inbred C57BL Chemotaxis Leukocyte 030104 developmental biology medicine.anatomical_structure Cancer cell Cancer research biology.protein 030215 immunology |
| Zdroj: | International Immunopharmacology. 63:66-73 |
| ISSN: | 1567-5769 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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