Human skin in the game

Abstract

Clinical and experimental observations in atopic dermatitis and psoriasis reveal new mechanisms of antiviral immunity and inflammation (Wolk et al., this issue; Kim et al., previous issue).

Figure 1. The production of antibacterial and antiviral proteins in psoriatic skin are regulated by different mechanisms

Antibacterial proteins can be induced by a variety of stimuli, including calcium, vitamin D, retinoic acid, microbial products and cytokines derived from both T cells and APC. In contrast, the production of antiviral proteins was closely linked to the production of IL-29, and to a lesser extent IFNγ, and the major source of IL-29 production was found to be Th17 cells resident within psoriatic skin lesions.

Figure 2. ILC2 initiate skin inflammation independent of the adaptive immune system in a mouse model of atopic dermatitis (AD)

Topical application of the vitamin D analog MC903 induces skin inflammation with histologic features reminiscent of human AD. ILC2s were observed in the skin and draining lymph nodes of treated mice and were found to mediate skin inflammation that was independent of T and B cells, ILCs and the canonical ILC2 cytokines IL-33 and IL-25, but was critically dependent on keratinocyte production of TSLP.