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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Cellimmuno; Molimmuno; Humdisease
ISSN (print) / ISBN
1074-7613
e-ISSN
1097-4180
Zeitschrift
Immunity
Quellenangaben
Band: 27,
Heft: 2,
Seiten: 296-307
Verlag
Cell Press
Verlagsort
Cambridge, Mass.
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed