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Yoon, Juhan; Leyva-Castillo, Juan Manuel; Wang, Guoxing; Galand, Claire; Oyoshi, Michiko K; Kumar, Lalit; Hoff, Sabine; He, Rui; Chervonsky, Alexander; Oppenheim, Joost J; Kuchroo, Vijay K; van den Brink, Marcel R M; Malefyt, Rene De Waal; Tessier, Philippe A; Fuhlbrigge, Robert; Rosenstiel, Philip; Terhorst, Cox; Murphy, George; Geha, Raif S
The Journal of experimental medicine, 09/2016, Volume: 213, Issue: 10Journal Article
Atopic dermatitis (AD) is a Th2-dominated inflammatory skin disease characterized by epidermal thickening. Serum levels of IL-22, a cytokine known to induce keratinocyte proliferation, are elevated in AD, and Th22 cells infiltrate AD skin lesions. We show that application of antigen to mouse skin subjected to tape stripping, a surrogate for scratching, induces an IL-22 response that drives epidermal hyperplasia and keratinocyte proliferation in a mouse model of skin inflammation that shares many features of AD. DC-derived IL-23 is known to act on CD4(+) T cells to induce IL-22 production. However, the mechanisms that drive IL-23 production by skin DCs in response to cutaneous sensitization are not well understood. We demonstrate that IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4(+) T cells that mediates epidermal thickening. We also show that IL-23 is released in human skin after scratching and polarizes human skin DCs to drive an IL-22 response, supporting the utility of IL-23 and IL-22 blockade in AD.
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