IL-17+ CD8+ T cells are defined by their ability to produce the pro-inflammatory cytokine IL-17A. These cells often also co-express one or several other cytokines including IFN-γ, TNF-α, IL-21, IL-22 and/or GM-CSF (the latter has not yet been reported in humans) , , , , . IL-17 can induce production of inflammatory mediators such as TNF-α, IL-6, IL-8 and chemokine (C-X-C motif) ligand 1 (CXCL1) by monocytes and fibroblasts, induce production of matrix metalloproteinases and promote osteoclastogenesis . IFN-γ, most frequently co-expressed in IL-17+ CD8+ T cells , , , is a pro-inflammatory cytokine typically expressed by some CD4+ and CD8+ T cells as well as some Natural Killer (NK) cells. IFN-γ is crucial for the induction of type I immunity and as described previously, IL-17A+ IFN-γ+ CD8+ T cells were found to produce higher levels of IFN-γ than IFN-γ single-producing T cells . TNF-α is also expressed by a broad range of immune cell types during inflammation and is capable of acting on a number of cell types including synergistically with IL-17 to promote activation of synovial fibroblasts and keratinocytes in the skin and joint of patients with RA and psoriasis , . IL-21 is a known driver of IL-17+ CD4+ T cell differentiation and is required for IL-17+ CD4+ T cell mediated pathogenesis in some models of inflammation in mice ; this cytokine may have a similar role in IL-17+ CD8+ T cell differentiation, though this is still to be fully investigated. IL-22 is produced by T cells and NK cells and has been shown to mediate keratinocyte differentiation and proliferation in psoriatic skin , . GM-CSF is a potent driver of inflammation via its actions on myeloid cells at the site of inflammation . Overall, the potential production of a broad range of pro-inflammatory cytokines by IL-17+ CD8+ T cells indicates these cells may contribute to pathogenesis via activation of neighbouring haematopoietic and stromal cells.