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Open Access Green as soon as Postprint is submitted to ZB.
Crosstalk between keratinocytes and adaptive immune cells in an IkappaBalpha protein-mediated inflammatory disease of the skin.
Immunity 27, 296-307 (2007)
Inflammatory diseases at epithelial borders develop from aberrant interactions between resident cells of the tissue and invading immunocytes. Here, we unraveled basic functions of epithelial cells and immune cells and the sequence of their interactions in an inflammatory skin disease. Ubiquitous deficiency of the I?B? protein (Ikba?/?) as well as concomitant deletion of Ikba specifically in keratinocytes and T cells (IkbaK5?/K5? lck?/lck?) resulted in an inflammatory skin phenotype that involved the epithelial compartment and depended on the presence of lymphocytes as well as tumor necrosis factor and lymphotoxin signaling. In contrast, mice with selective ablation of Ikba in keratinocytes or lymphocytes showed inflammation limited to the dermal compartment or a normal skin phenotype, respectively. Targeted deletion of RelA from epidermal keratinocytes completely rescued the inflammatory skin phenotype of Ikba?/? mice. This finding emphasizes the important role of aberrant NF-?B activation in both keratinocytes and lymphocytes in the development of the observed inflammatory skin changes.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cellimmuno; Molimmuno; Humdisease
ISSN (print) / ISBN
1074-7613
e-ISSN
1097-4180
Journal
Immunity
Quellenangaben
Volume: 27,
Issue: 2,
Pages: 296-307
Publisher
Cell Press
Publishing Place
Cambridge, Mass.
Reviewing status
Peer reviewed