Increased IL-17A induces IgG memory B cells to produce IgE by class-switch recombination, forming immune complexes containing soluble IgE with psoriasis-associated autoantigens; these are presented to plasmacytoid (p) DCs via FcεRI, activating pDCs to trigger inflammatory cytokine responses, including IFN-α, IL-6, IL-8, and TNF, involved in the development and maintenance of inflammatory processes in psoriatic lesions (15–17). Here, TNF is linked to psoriasis.