IL17A and psoriasis: Together, these findings suggest that IL-17A and TNF-α act through distinct mechanisms to regulate downstream gene expression, with the IL-23/IL-17A axis at the core of psoriasis pathogenesis, and TNF-α playing a more ancillary role in promoting inflammation through synergism with IL-17A and through development and maturation of myeloid dendritic cells [6, 31].