Radiation-induced CXCL16 release by breast cancer cells attracts effector T cells.

摘要: Recruitment of effector T cells to inflamed peripheral tissues is regulated by chemokines and their receptors, but the factors regulating recruitment tumors remain largely undefined. Ionizing radiation (IR) therapy a common treatment modality for breast other cancers. Used as cytocidal agent proliferating cancer cells, IR in combination with immunotherapy has been shown promote immune-mediated tumor destruction preclinical studies. In this study we demonstrate that markedly enhanced secretion mouse human CXCL16, chemokine binds CXCR6 on Th1 activated CD8 plays an important role sites inflammation. Using poorly immunogenic model cancer, found irradiation increased migration CD8(+)CXCR6(+) vitro vivo. CXCR6-deficient mice showed reduced infiltration impaired regression following local Abs blocking negative regulator cell activation, CTLA-4. These results provide first evidence can induce proinflammatory chemotactic recruit antitumor cells. The ability convert into "inflamed" could be exploited overcome obstacles at phase immune response improve therapeutic efficacy immunotherapy.