**3.2 Th17/IL-17: crucial players in psoriasis**

Psoriasis is considered as a "IL-17 centric" disease with a preponderance of pathogenic Th17 cells [28]. Psoriatic Th17 cells produce high levels of IL-17 (A to F), IL-26, IL-29 and IL-22 that synergistically act as transcriptional enhancers of many keratinocyte-expressed genes. IL-26 is linked with increased vascularisation while IL-29 regulates the expression of antiviral proteins [29, 30]. IL-17 induced inflammatory effects are not only limited to cutaneous plaques but also to more distant alterations in numerous different cell types that are responsible for producing systemic inflammatory effects and psoriasis-associated co-morbidities [31]. (**Figure 1**) IL-17 mediated psoriasogenicity is also linked in part to its synergism with other cytokines such as tumor necrosis factor (TNF)-α, IL-22, IL-23, IL-1β, IL-6, TGF-β across various organ systems [32].
