Figure 5. CXCR3 deficiency results in improved survival and decreased TCF1 downregulation of TCF1⁺ cells and decreased terminal differentiation of Teff-l.

(A) CXCR3 expression normalized to expression on Tstem-l and the frequency of CXCR3⁺ cells on distinct subsets of GP276-specific cells on d24 of Cl13 infection in WT mice. (B-F) Congenically marked cell tracker violet (CTV)-labelled CX₃CR1⁻Ly108⁺CD44⁺PD1⁺ CD8⁺ T cells (Tstem-l) from chronically infected CD45.2 WT, or CD45.2 Cxcr3^−/− mice were adoptively transferred into infection matched CD45.1 recipient. (B) Experimental scheme. (C) Flow cytometry plots of recovered cells. (D-F) The total number of recovered cells (D), percentage of divided cells (E), and phenotype of divided cells (F) among adoptively transferred WT and Cxcr3^−/− cells on d8 post-transfer. (G-H) Flow cytometry plots and quantification of CD101 expression on CXCR3⁻ and CXCR3⁺ Teff-l on d24 pi. with Cl13 in WT and Cxcl10^−/− mice in spleen (G) and liver (H). (B, I-J) Congenically marked CX₃CR1⁺Ly108⁻PD1⁺ CD8⁺ T cells (Teff-l) from chronically infected CD45.2 WT or CD45.2 Cxcr3^−/− mice were adoptively transferred into infection matched WT CD45.1 recipient that were treated with 150μg of CD4 depleting mAb one day before and after infection to induce stable viremia. (B) Experimental scheme. (I-J) Flow cytometry plots and frequency of CD101⁺ cells among transferred WT and Cxcr3^−/− cells recovered from spleen (I) and liver (J) on d14 post-transfer. Data are from at least two independent experiments (n=3–4 per time point). Data in A,G and H were analyzed with an ordinary one-way Anova test with Tukey’s multiple comparison test; data in D-E, I-J with unpaired Student’s t-test; and data in F with an ordinary one-way Anova test Sidak’s multiple comparison test; *, P < 0.05; **, P < 0.01; ***, P < 0.001. See also Figure S3.