CXCR3 deficiency alters effector CD8⁺ T cell phenotype to MPECs in vivo. (A–E) 1 d after transfer of mixed CXCR3^−/− and WT OT-I cells, recipient mice were infected with VV-OVA as in Fig.1 B. OT-I cells in spleen were analyzed at day 7 after infection. Data represent three independent experiments (n = 3–4 per time point). (A) Expression of CD127 and KLRG1. (B) Percentage of CD127^hi KLRG1^lo cells among OT-I cells. Bars represent mean. *, P < 0.0001. (C) Expression of CD27 and CD122. Numbers to the right of CD122 plots show MFI and MFI ratio of CXCR3^−/− to WT. (D) Intracellular granzyme B expression. Numbers below granzyme B plots indicate MFI. (E) Intracellular TNF, IL-2, and IFN-γ production. (F) Naive CXCR3^−/− and WT OT-I cells (mixed in a 1:1 ratio) were co-cultured with DC-OVA in the presence or absence of CXCR3 ligands (CXCL9, CXCL10, or CXCL11) for 7 d. (G) Phenotype and cytokine production profiles of OT-I cells on day 7. Representative data at 100 ng/ml ligand stimulation. (H and I) Cultured OT-I cells were transferred into WT mice. (H) Percentage of CXCR3^−/− (bottom) and WT (top) cells in total OT-I populations at days 1 and 42 after transfer. (I) Number of in vitro–generated CTL at days 1 and 42 after transfer. Data are shown as mean ± SEM. (F–I) Data are representative of two independent experiments (n = 3).