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. 2007 Sep 20;117(10):3087–3096. doi: 10.1172/JCI30605

Figure 3. Ex vivo analysis of OT-I and OT-II activation following vaccination with OVA-GMLs.

Figure 3

(A) Structure of the retroviral vector OVA-CSM. (B) Twenty-four hours after the infusion of CFSE-labeled OT-I T cells, mice were given mock-GMLs (Mock) or OVA-GMLs from WT (OVA WT) or β2m–/– (OVA β2m–/–) mice. Density dot plots (CFSE, left panels) show OT-I proliferation following treatments. Histograms show the expression of CD44 and downregulation of CD62L. (C) OT-I T cells from treated mice were restimulated in vitro with OVA257–264–loaded splenocytes and tested for IFN-γ release against pulsed or unpulsed RMA cells. In vitro–activated OT-I T cells were used as positive control. (D) Twenty-four hours after the infusion of CFSE-labeled OT-II T cells, mice were given mock- or OVA β2m–/–GMLs. Density dot plots show OT-II proliferation following treatment with OVA β2m–/– GMLs (CFSE, left panels). Histograms show the expression of CD44 and downregulation of CD62L. Data are representative of 3 (B) or 2 (D) experiments performed on splenocytes of 2 mice/group. (E) B16-OVA–bearing mice were transferred with OT-I T cells and then treated with mock- or OVA-GMLs from WT or β2m–/– mice. *P < 0.05, **P < 0.005; Student’s t test. (F) Mice adoptively transferred with OT-I T cells were challenged with mock- or OVA-GMLs from WT and β2m–/– mice. Forty days later, mice were challenged with B16-OVA cells and followed up. **P < 0.005, †P < 0.0005; Student’s t test. Data are representative of 3 (E) or 2 (F) experiments with 5 mice/group.