Our recent data also raise the possibility that disrupted tolerance and a switch from non-inflammatory to inflammatory Th17/IL17 milieu may have special role in the development of SGR localized inflammatory skin diseases, since in SGR skin during steady-state a homeostatic, probably tolerogenic TSLP epidermal expression was detected while a significant loss of this TSLP together with prominent influx of inflammatory DCs and inflammatory Th17/Th1 cells with IL-17/interferon-γ cytokine milieu were observed during the development of rosacea (7). Here, IL17A is linked to inflammatory skin disease.