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The chemokine receptor CXCR6 is expressed on different T cell subsets and up-regulated following T cell activation. CXCR6 has been implicated in the localization of cells to the liver due to the constitutive expression of its ligand CXCL16 on liver sinusoidal endothelial cells. Here, we analyzed the role of CXCR6 in CD8 +  T cell responses to infection of mice with  Listeria monocytogenes . CD8 +  T cells responding to listerial antigens acquired high expression levels of CXCR6. However, deficiency of mice in CXCR6 did not impair control of the  L. monocytogenes  infection. CXCR6-deficient mice were able to generate listeria-specific CD4 +  and CD8 +  T cell responses and showed accumulation of T cells in the infected liver. In transfer assays, we detected reduced accumulation of listeria-specific CXCR6-deficient CD8 +  T cells in the liver at early time points post infection. Though, CXCR6 was dispensable at later time points of the CD8 +  T cell response. When transferred CD8 +  T cells were followed for extended time periods, we observed a decline in CXCR6-deficient CD8 +  T cells. The manifestation of this cell loss depended on the tissue analyzed. In conclusion, our results demonstrate that CXCR6 is not required for the formation of a T cell response to  L. monocytogenes  and for the accumulation of T cells in the infected liver but CXCR6 appears to influence long-term survival and tissue distribution of activated cells.

The Function of the Chemokine Receptor CXCR6 in the T Cell Response of Mice against Listeria monocytogenes