Three decades of psoriasis research: Where has it led us?

被引:31
作者
Sabat, Robert [1 ]
Sterry, Wolfram [2 ]
Philipp, Sandra [1 ]
Wolk, Kerstin [1 ]
机构
[1] Univ Hosp Charite, Interdisciplinary Grp Mol Immunopathol Dermatol M, D-10117 Berlin, Germany
[2] Univ Hosp Charite, Dept Dermatol & Allergy, D-10117 Berlin, Germany
关键词
D O I
10.1016/j.clindermatol.2007.08.002
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Psoriasis is a common chronic skin disease. Its pathogenesis has intensively been investigated in the last 3 decades. In the 1970s, the observed increased proliferation of keratinocytes and their altered differentiation were considered to be the most important signs and causes of psoriatic skin lesions. Since the early 1980s. T cells slid into the focus of psoriasis research. It was then postulated that a subpopulation of T cells, so-called T1 cells, and their prominent cytokine interferon-gamma, had a dominant role in the pathogenesis of psoriasis. In the last decade, new data regarding macrophages and dendritic cells and the high therapeutic success of anti-tumor necrosis factor alpha biologics led to the assumption that antigen -presenting cells are important not only in the induction of psoriasis but also in its maintenance. The knowledge gained over the past 3 decades let us postulate that psoriasis is an immunologically induced, overshot, regeneration-like reaction of the skin in which various cells play a dominant role at different stages. This hypothesis is also supported by the very recent discoveries about interleukin (IL)-22, IL-20, and IL-23. (c) 2007 Elsevier Inc. All rights reserved.
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收藏
页码:504 / 509
页数:6
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