Crosstalk between keratinocytes and adaptive immune cells in an IkappaBalpha protein-mediated inflammatory disease of the skinстатья

Статья опубликована в высокорейтинговом журнале

Информация о цитировании статьи получена из Scopus, Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 14 сентября 2013 г.

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1. Rebholtz_Immunity_2007.pdf Rebholtz_Immunity_2007.pdf 3,4 МБ 2 августа 2013 [snedos]

[1] Crosstalk between keratinocytes and adaptive immune cells in an ikappabalpha protein-mediated inflammatory disease of the skin / B. Rebholz, I. Haase, B. Eckelt et al. // Immunity. — 2007. — Vol. 27, no. 2. — P. 296–307. Inflammatory diseases at epithelial borders develop from aberrant interactions between resident cells of the tissue and invading immu- nocytes. Here, we unraveled basic functions of epithelial cells and immune cells and the sequence of their interactions in an inflamma- tory skin disease. Ubiquitous deficiency of the IkBa protein (IkbaD/D) as well as concomitant deletion of Ikba specifically in keratinocytes and T cells (IkbaK5D/K5D lckD/lckD) 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 compart- ment or a normal skin phenotype, respectively. Targeted deletion of RelA from epidermal kera- tinocytes completely rescued the inflammatory skin phenotype of IkbaD/D mice. This finding emphasizes the important role of aberrant NF-kB activation in both keratinocytes and lym- phocytes in the development of the observed inflammatory skin changes. [ DOI ]

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