In particular, the main drivers of these differences were the populations of CD8+ Ag+ T cells CD107a+IFN-γ+IL-2−IL-17−TNF−, and CD107a−IFN-γ+IL-2−IL-17−TNF−, the one able to produce CD107a+IFN-γ+IL-2−IL-17−TNF+ whose percentages were higher in PR patients when compared to age-matched HD (Figure 4C,D). Here, CD8A is linked to Huntington disease.