IL-23 is often used to expand human IL-17+ CD4+ T cells , . IL-23 addition to hapten-primed mouse CD8+ T cell and dendritic cell co-cultures induced IL-17 production , yet IL-23 alone only slightly induced Il17a expression in mouse naïve CD8+ T cell cultures . Thus, IL-23 may maintain the IL-17+ CD8+ T cell phenotype rather than drive differentiation, similar to its role in IL-17+ CD4+ T cells . In humans, a role for IL-23 in IL-17+ CD8+ T cell differentiation is not yet elucidated, however one study revealed that heterozygous carriers of the R381Q IL23R variant exhibited reduced IL-17+ CD8+ T cell frequencies compared to carriers of the common variant , indicating a potential role of IL-23 in human IL-17+ CD8+ T cell development. IFN-γ neutralisation expanded mouse IL-17+ CD8+ T cells in vitro , ,  and α-IFN-γ mAb removal from the polarising cocktail also containing IL-1β, IL-2, IL-6, IL-21, IL-23, TGF-β and α-IL-4 mAb, reduced IL-17+ CD8+ T cell frequencies . These data indicate that IFN-γ reduces IL-17+ CD8+ T cell expansion, as seen in mouse IL-17+ CD4+ T cell studies . In support of this, Type I IFN signalling-deficient mice (used to inhibit IFN-γ+ CD8+ T cell induction) treated with neutralising IFN-γ Abs showed higher IL-17+ CD8+ T cell levels in vivo, as compared to wild type mice . IL-17+ CD8+ T cell frequencies were also expanded in vivo when allogeneic mice were injected with α-IFN-γ mAb 7 days post-stem cell transplant . Additionally, higher IL-17+ CD8+ T cell frequencies were reported in IFN-γ-deficient OT-I mice compared to wild-type mice , further indicating that IFN-γ inhibition in vivo enhances IL-17 production by CD8+ T cells in mice. IFN-γ was neutralised in one in vitro human IL-17+ CD8+ T cell differentiation study , however further investigations are required to establish its exact role in the human context.