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Publication : IL-33 induces skin inflammation with mast cell and neutrophil activation.

First Author  Hueber AJ Year  2011
Journal  Eur J Immunol Volume  41
Issue  8 Pages  2229-37
PubMed ID  21674479 Mgi Jnum  J:176814
Mgi Id  MGI:5292783 Doi  10.1002/eji.201041360
Citation  Hueber AJ, et al. (2011) IL-33 induces skin inflammation with mast cell and neutrophil activation. Eur J Immunol 41(8):2229-37
abstractText  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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