Type I interferons in psoriasis

Psoriasis is a chronic skin disease characterized by inflammation and abnormal epidermal proliferation mediated by infiltrated T cells, dendritic cells, and inflammatory cytokines. It can be considered a disease caused by the impaired cross-talk between the immune system and the structural cells of the skin. Both genetic components and environmental factors, especially pathogenic infections, can predispose patients to the disease or induce its onset.Psoriasis is generally regarded as a Th1 cytokine-reactive disease, in which pro-inflammatory cytokines such as interferon (IFN)-γ; interleukin (IL)-12, -17, and -23; and tumor necrosis factor (TNF)-α play a key role, and therapies targeting TNF-α and IL-12, -17, and -23 have shown significant clinical benefit. It has also been shown that type I IFN may be a key link between non-specific stimuli and pathogenic consequences. Recently, an elevated type I IFN signature was identified in lesional skin of subjects with psoriasis. Accumulating evidence suggests that type I IFN, although indispensable, might play a secondary role to other Th1 cytokines in the pathogenesis of psoriasis. In this chapter, we provide a detailed review of the role of type I IFN in psoriasis with regard to its possible involvement in the pathogenesis of the disease, the activation of keratinocytes and T cells, and its potential synergistic cooperation or cross-regulation with Th1 cytokines like TNF-α.