Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins (Nature, 2005, 437:369-375)

報告日期: 2006/03/28
報告時間: 16:00/16:50
報告學生: 吳金漢
講評老師: 洪建中
附件下載:

 

Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins

 

Nature, 437369375, 2005

 

Speaker : 吳金漢                  Time3/28/2006

Commentator : 洪建中 老師        PlaceRoom 602

 

Abstract:

Psoriasis, a common inflammatory disease of skin and joints, has been variously regarded as an immune disorder that affects the skin, or a skin disorder with immunological consequences. In the absence of a good animal model it has been difficult to be certain. Starting from the discovery that epidermal keratinocytes in human psoriatic lesions have reduced expression of transcription factor JunB, which was a component of the AP-1 and is known to regulate cell proliferation and differentiation. In this paper, the authors designed inducible, conditional, and double-knockout mice for JunB and c-Jun alleles in the epidermis of adult mice. After tamoxifen treatment, JunB/c-Jun double- knockout mice closely resembled the skin lesions of patients with psoriasis. Genetic evidence shows that skin lesions develop independently of immune cells and that the arthritis is primarily mediated by TNF signalling. Immune cells seem to act merely as amplifiers of the inflammatory response.

 

Reference:

Zenz R, Wagner EF.Jun signalling in the epidermis: From developmental defects to psoriasis and skin tumors. Int J Biochem Cell Biol. Available online 20 December 2005.

 

Mehic D, Bakiri L, Ghannadan M, Wagner EF, Tschachler E. Fos and jun proteins are specifically expressed during differentiation of human keratinocytes. J Invest Dermatol. 124:212-20, 2005.