Suppression of autoimmune disease after vaccination with autoreactive T cells that express Qa-1 peptide complexes
J. Clin. Invest. Vily Panoutsakopoulou, et al. 113:1218 doi:10.1172/JCI20772 [Go to this article.]

Figure 2
V_β expression and TCV. (A) TCR V_β8⁺ CD4 cells protect from development of HSK. C.AL-20 mice were vaccinated with CD4 cells (as described in Methods) sorted according to TCR-V_β expression (V_β8⁺, filled circles; V_β8⁻, open squares; V_β2⁺, open circles). All mice were ocularly infected with HSV-1 (KOS) and scored for HSK. Each group consisted of ten mice, and results are representative of three independent experiments. (B) BALB/c mice were vaccinated with cells of either a TCR V_β8⁺ CD4 T cell clone reactive to a corneal antigen (C1-6, open circles), or a CD4 T cell clone reactive to an OVA-derived peptide (DO11.10; open squares), or a TCR V_β6⁺ CD4 T cell clone reactive to an OVA-derived peptide (O3; filled square), or were unvaccinated controls (filled circle). All mice were ocularly infected with HSV-1 (KOS) and scored for HSK. Each group consisted of ten mice, and results are representative of four independent experiments. (C) Binding of a TCR-derived V_β8.1 peptide to Qa-1 renders O3 cells protective. C.AL-20 mice were vaccinated with pure cells of the TCR V_β6⁺ CD4 T cell clone O3 (open squares) or O3 cells incubated with a TCR-derived V_β8.1 peptide (open circles) or the mutated peptide L9D (filled circles). Two weeks later, all mice were ocularly infected with HSV-1 (KOS) and scored for HSK. Each group consisted of ten mice, and results are representative of three independent experiments.