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IL-33 is regulated by TNF-α in normal and psoriatic skin

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Abstract

Interleukin-33 (IL-33) is the most recently discovered IL-1 family member. Considered an endogenous “alarmin” released by necrotic cells in response to tissue injury or damage, IL-33 is constitutively expressed in tissues exposed to the environment, where endothelial and epithelial cells constitute its major sources. Several findings reported that pro-inflammatory stimuli, such as IFN-γ and TNF-α, as well as IL-17, can induce IL-33 expression in normal human epidermal keratinocytes. In the present study, we deeply investigated the relation between IL-33 and TNF-α, by employing the whole skin as study model. TNF-α dose- and time-dependently induced IL-33 gene expression in ex vivo healthy skin organ culture. Similarly, TNF-α significantly increased IL-33 mRNA expression in normal human epidermal sheets. Moreover, IL-33 was enhanced in psoriatic skin and anti-TNF-α therapy was able to significantly reduce it. The biology of IL-33 is gaining in complexity, and this molecule is now known to have additional roles beyond its original description. In particular, we can assess that IL-33 is regulated by TNF-α in normal and psoriatic skin.

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Correspondence to Anna Balato.

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Balato, A., Di Caprio, R., Canta, L. et al. IL-33 is regulated by TNF-α in normal and psoriatic skin. Arch Dermatol Res 306, 299–304 (2014). https://doi.org/10.1007/s00403-014-1447-9

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  • DOI: https://doi.org/10.1007/s00403-014-1447-9

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