Figure 3. CD8⁺ TILs from patients BC7 and BC9 recognize class I–restricted mutated peptides.

(A) IFNγ ELISPOT showing BC7 TIL recognition of the mutant version (H-RAREEIVAHIAL-OH) of RNA-binding protein MEX3B (mutation E→V at position 7) but not the wild-type form nor the negative control HIV-gag. The quantification of BC7 ELISPOT reactivity against mutant MEX3B is shown as number of spots/10⁶ TILs. A TIL-alone control is also included; n = 2 independent experiments (B) IFNγ ELISPOT demonstrating BC9 TIL recognition of the mutant version (H-FAFVTENTY-OH) of G2/mitotic-specific cyclin-B1 (mutation D→E at position 6) as compared to the wild-type form. Quantification of BC9 ELISPOT reactivity against mutant cyclin-B1 is shown as number of spots/5×10⁵ TIL; n = 3 independent experiments. For A) and B) the average number of spot is shown per condition as a label over the bar graphs. (C) IFNγ intracellular staining of BC9 TILs stimulated with either WT or mutant cyclin-B1 showing that mutated G2/mitotic-specific cyclin-B1–specific CD8⁺ T cells constituted over 50% of BC9 TILs. IFNγ expression is gated on live, CD3⁺CD4⁻CD8⁺ TILs.