Scientists have previously taken two different views on what triggers psoriasis, an inflammatory disease of the skin and joints. Some people have regarded it as an immune disorder that affects the skin (the 'inside-out' hypothesis) whereas others have seen it as a skin disorder with immunological repercussions (the 'outside-in' hypothesis). But deciding between these two ideas has remained difficult in the absence of a mouse model.
A new finding, described in the 15 Sept. 2005 issue of Nature (Vol. 437, No. 7057, pp. 369-375), addresses this problem: Erwin Wagner and his colleagues found that cells in human psoriatic lesions have decreased expression of the gene JUNB. The team has now been able to engineer mice that lack the analogous mouse gene. These animals develop a skin disease almost identical to psoriasis in people. Genetic evidence from the study shows that the skin lesions develop independently of immune cells, supporting the 'outside-in' hypothesis.
Erwin F. Wagner (Research Institute of Molecular Pathology, Vienna, Austria)
(C) Nature press release.
Message posted by: Trevor M. D'Souza
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