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. 2016 Apr 14;7(4):e2193. doi: 10.1038/cddis.2016.83

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Copyright © 2016 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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DNT homed to the injured liver via the CXCR3-CXCL9/CXCL10 interaction to exert a protective function. ConA-induced DNT (GFP⁺) migrated to the injured liver after ConA administration (a). The migration of GFP⁺DNT was significantly reduced with increasing concentrations of CXCR3-neutralizing mAb tested by in vitro migration assay (b), and the migration inhibition was dose dependent (c). Real-time PCR results showed that mRNA of the CXCR3 ligand CXCL9/10, but not CXCL11, was highly expressed in the injured livers (d). The results reported are representative of three experiments with similar results. **P<0.01, *P<0.05