The most definitive feature of human IL-17+ CD8+ T cells is their ability to produce the pro-inflammatory cytokine IL-17A (IL-17) but concurrent expression of several other cytokines has been shown. The most well-described of these is the pro-inflammatory cytokine IFN-γ, which is found to be co-expressed with IL-17 in cultured IL-17+ CD8+ T cells from healthy blood  and psoriatic plaques . Furthermore IL-17/IFN-γ dual producers derived from the liver tissue of patients with hepatitis C infection produced higher levels of IFN-γ than IFN-γ+ CD8+ T (Tc1) cells, indicating these cells may represent a population with higher pro-inflammatory potential . In addition, several other pro-inflammatory cytokines such as tumour necrosis factor alpha (TNF-α), IL-21 and IL-22 have been shown to be co-expressed with IL-17 by human and mouse IL-17+ CD8+ T cells , , , . Granulocyte macrophage colony stimulating factor (GM-CSF) co-expression has also been reported, at least in mouse . Moreover, evidence for lack of co-expression of the anti-inflammatory cytokine IL-10 by IL-17+ CD8+ T cells in mice supports classification of IL-17+ CD8+ T cells as pro-inflammatory . At the molecular level, studies into the phenotype of human IL-17+ CD8+ T cells have been restricted, with only one study showing that RORC (encoding retinoic acid receptor-related orphan receptor gamma; RORγt) gene expression was increased in psoriatic skin IL-17+ CD8+ T cells, compared to IL-17- CD8+ T cells, which in contrast expressed higher expression of TBX21 (encoding T-Bet) . This is supported by data from mouse models where Rorc has been shown to be expressed at a high level in spleen and lymph node (LN) derived IL-17+ CD8+ T cells differentiated in vitro , , . RORγt has been extensively implicated in the development and function of IL-17+ CD4+ T cells, and these data suggest that IL-17+ CD8+ T cell phenotype and function may be defined by a similar mechanism.