Figure 4.
CXCR3−/− effector CD8+ T cells show resistance to cell death in the late effector phase. (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. (A) Recipient mice were i.p. injected with BrdU 24 h before sacrifice. Representative histograms gated on CXCR3−/− or WT OT-I cells in the spleen show BrdU incorporation. Numbers indicate the percentage of BrdU-positive population. (B) Ratio of percentage of BrdU-positive population of CXCR3−/− to WT OT-I cells. Data are shown as mean ± SEM. *, P < 0.001; **, P < 0.0001. (C–E) Apoptotic balance of CXCR3−/− and WT OT-I cells at days 5 and 7 after infection was evaluated by measuring percentage of Bcl-2+ and annexin V+ cells (C), pan-caspase activity (D), and TUNEL assay (E). Data are shown as mean ± SEM. *, P < 0.05. (F) CXCR3−/− and WT effector OT-I cells were generated in separate hosts and recovered from the spleen on day 6 after VV-OVA infection. A 1:1 mixture of CXCR3−/− and WT OT-I cells was transferred into naive hosts and contraction of both OT-I cell populations was compared. (G) Representative plots showing the percentage of CXCR3−/− (bottom) and WT (top) cells out of the total OT-I populations at days 1 and 41 after transfer. (H) Number of OT-I cells at days 1 and 41 after transfer. Data are shown as mean ± SEM. *, P < 0.05. Data represent three (A–C) or two (D–H) independent experiments (n = 3–4 per time point).