In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-12-23)
Abstract:
Psoriasis is an inflammatory disorder that causes red, flaky patches of skin. The disease affects around 2% of the world’s population, and is most common in people of northern European descent. TNF is one of the key proteins in the development of psoriasis and drugs that inhibit TNF have been very successful in the treatment of this disease. However, these drugs are expensive and for unknown reasons at least 10% of patients do not respond to them. Attempts to develop better drugs for psoriasis would be assisted by an improved understanding of this disease in terms of the genes and proteins involved. Etemadi et al. set out to obtain a more detailed molecular understanding of this disease by developing new mouse models of the condition. Mice were genetically engineered such that a key gene was deleted specifically from the skin cells that form the main barrier to the environment. These mice demonstrated that defects in skin cells called keratinocytes, rather than defects in the immune response, could lead to a psoriasis-like disease. Etemadi et al. also showed that the skin cells with this genetic defect die in the presence of TNF and this cell death in mice caused a rapidly-appearing form of psoriasis. However, in the absence of TNF the mice still developed psoriasis, albeit more slowly. In this case, the condition was due to an excessive activation of a protein called NF-κB, which is known to play a role in maintaining balance in the immune system and in psoriasis. These findings reveal how keratinocytes, cell death and inflammation can directly contribute to psoriasis-like conditions in mice. The next challenge will be to determine whether these findings can be used to help patients with this condition.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.10592.001
DOI:
10.7554/eLife.10592.002
DOI:
10.7554/eLife.10592.003
DOI:
10.7554/eLife.10592.004
DOI:
10.7554/eLife.10592.005
DOI:
10.7554/eLife.10592.006
DOI:
10.7554/eLife.10592.007
DOI:
10.7554/eLife.10592.008
DOI:
10.7554/eLife.10592.009
DOI:
10.7554/eLife.10592.010
DOI:
10.7554/eLife.10592.011
DOI:
10.7554/eLife.10592.012
DOI:
10.7554/eLife.10592.013
DOI:
10.7554/eLife.10592.014
DOI:
10.7554/eLife.10592.015
DOI:
10.7554/eLife.10592.017
DOI:
10.7554/eLife.10592.018
DOI:
10.7554/eLife.10592.016
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2015
detail.hit.zdb_id:
2687154-3
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