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  • Title: IL-26 Potentiates Type 2 Skin Inflammation in the Presence of IL-1β.
    Author: Bier K, Senajova Z, Henrion F, Wang Y, Bruno S, Rauld C, Hörmann LC, Barske C, Delucis-Bronn C, Bergling S, Altorfer M, Hägele J, Knehr J, Junt T, Roediger B, Röhn TA, Kolbinger F.
    Journal: J Invest Dermatol; 2024 Jul; 144(7):1544-1556.e9. PubMed ID: 38237730.
    Abstract:
    Atopic dermatitis (AD) is a debilitating inflammatory skin disorder. Biologics targeting the IL-4/IL-13 axis are effective in AD, but there is still a large proportion of patients who do not respond to IL-4R blockade. Further exploration of potentially pathogenic T-cell-derived cytokines in AD may lead to new effective treatments. This study aimed to investigate the downstream effects of IL-26 on skin in the context of type 2 skin inflammation. We found that IL-26 alone exhibited limited inflammatory activity in the skin. However, in the presence of IL-1β, IL-26 potentiated the secretion of TSLP, CXCL1, and CCL20 from human epidermis through Jak/signal transducer and activator of transcription signaling. Moreover, in an in vivo AD-like skin inflammation model, IL-26 exacerbated skin pathology and locally increased type 2 cytokines, most notably of IL13 in skin T helper cells. Neutralization of IL-1β abrogated IL-26-mediated effects, indicating that the presence of IL-1β is required for full IL-26 downstream action in vivo. These findings suggest that the presence of IL-1β enables IL-26 to be a key amplifier of inflammation in the skin. As such, IL-26 may contribute to the development and pathogenesis of inflammatory skin disorders such as AD.
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