Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 41, Issue 8, Pages 2229-2237Publisher
WILEY
DOI: 10.1002/eji.201041360
Keywords
Cytokine; Inflammation; Interleukin; Psoriasis
Categories
Funding
- German research foundation (DFG)
- BHF [FS/08/035/25309]
- British Heart Foundation [FS/08/035/25309] Funding Source: researchfish
- Chief Scientist Office [CZB/4/697] Funding Source: researchfish
- Medical Research Council [G9818261, G0801198, G0901113] Funding Source: researchfish
- MRC [G0801198, G9818261, G0901113] Funding Source: UKRI
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Psoriasis is a common chronic autoimmune condition of the skin characterized by hyperplasia of epidermal keratinocytes associated with pro-inflammatory cytokines. IL-33 is a new member of the IL-1 superfamily that signals through the ST2 receptor and was originally defined as an inducer of T helper 2 (Th2) cytokines. Recently, broader immune activatory potential has been defined for IL-33 particularly via mast cell activation and neutrophil migration. Here, we show that ST2(-/-) mice exhibit reduced cutaneous inflammatory responses compared with WT mice in a phorbol ester-induced model of skin inflammation. Furthermore, injections of IL-33 into the ears of mice induce an inflammatory skin lesion. This inflammatory response was partially dependent on mast cells as mast cell-deficient mice (Kit(W-sh/W-sh)) showed delayed responses to IL-33. IL-33 also recruited neutrophils to the ear, an effect mediated in part by increased production of the chemokine KC (CXCL1). Finally, we show that IL-33 expression is up-regulated in the epidermis of clinical psoriatic lesions, compared with healthy skin. These results therefore demonstrate that IL-33 may play a role in psoriasis-like plaque inflammation. IL-33 targeting may provide a new treatment strategy for psoriasis.
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