Psoriasis pathophysiology: current concepts of pathogenesis

被引:370
作者
Krueger, JG
Bowcock, A
机构
[1] Rockefeller Univ, Invest Dermatol Lab, New York, NY 10021 USA
[2] Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA
关键词
D O I
10.1136/ard.2004.031120
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Psoriasis vulgaris is a common skin disorder characterised by focal formation of inflamed, raised plaques that constantly shed scales derived from excessive growth of skin epithelia[ cells, The disease is defined by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils, and other types of leuco e in affected skin. In a relatively short period, psoriasis vulgaris has been conceptualised as a T lymphocyte mediated autoimmune disease and new biological therapies that forget T cells hove just entered routine clinical practice. Similarly, rapid progress has been made towards dissecting cellular and molecular pathways of inflammation that contribute to disease pathogenesis. This short review presents current pathogenic concepts that have emerged from genetic, genomic, and cellular information obtained in basic studies and from clinical studies of selective immune targeting drugs.
引用
收藏
页码:30 / 36
页数:7
相关论文
共 52 条
[1]   Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells [J].
Abrams, JR ;
Kelley, SL ;
Hayes, E ;
Kikuchi, T ;
Brown, MJ ;
Kang, SW ;
Lebwohl, MG ;
Guzzo, CA ;
Jegasothy, BV ;
Linsley, PS ;
Krueger, JG .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (05) :681-693
[2]   Cellular responses to interferon-gamma [J].
Boehm, U ;
Klamp, T ;
Groot, M ;
Howard, JC .
ANNUAL REVIEW OF IMMUNOLOGY, 1997, 15 :749-795
[3]   Overexpression of CD1d by keratinocytes in psoriasis and CD1d-dependent IFN-γ production by NK-T cells [J].
Bonish, B ;
Jullien, D ;
Dutronc, Y ;
Huang, BB ;
Modlin, R ;
Spada, FM ;
Porcelli, SA ;
Nickoloff, BJ .
JOURNAL OF IMMUNOLOGY, 2000, 165 (07) :4076-+
[4]   The genetics of psoriasis, psoriatic arthritis and atopic dermatitis [J].
Bowcock, AM ;
Cookson, WOCM .
HUMAN MOLECULAR GENETICS, 2004, 13 :R43-R55
[5]   Spontaneous development of psoriasis in a new animal model shows an essential role for resident T cells and tumor necrosis factor-α [J].
Boyman, O ;
Hefti, HP ;
Conrad, C ;
Nickoloff, BJ ;
Suter, M ;
Nestle, FO .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 199 (05) :731-736
[6]   Direct inhibition of the signaling functions of the mammalian target of rapamycin by the phosphoinositide 3-kinase inhibitors, wortmannin and LY294002 [J].
Brunn, GJ ;
Williams, J ;
Sabers, C ;
Wiederrecht, G ;
Lawrence, JC ;
Abraham, RT .
EMBO JOURNAL, 1996, 15 (19) :5256-5267
[7]   Generation of antigen-loaded dendritic cells in a serum-free medium using different cytokine combinations [J].
Büchler, T ;
Hajek, R ;
Bourkova, L ;
Kovarova, L ;
Musilova, R ;
Bulikova, A ;
Doubek, M ;
Svobodnik, A ;
Mareschova, I ;
Vanova, P ;
Tuzova, E ;
Vidlakova, P ;
Vorlicek, J ;
Penka, M .
VACCINE, 2003, 21 (9-10) :877-882
[8]  
Curry JL, 2003, ARCH PATHOL LAB MED, V127, P178
[9]   Comparison of the distribution and numbers of antigen-presenting cells among T-lymphocyte-mediated dermatoses -: CD1a+, factor XIIIa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease [J].
Deguchi, M ;
Aiba, S ;
Ohtani, H ;
Nagura, H ;
Tagami, H .
ARCHIVES OF DERMATOLOGICAL RESEARCH, 2002, 294 (07) :297-302
[10]   CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: Blood and skin comparisons by flow cytometry [J].
Ferenczi, K ;
Burack, L ;
Pope, M ;
Krueger, JG ;
Austin, LM .
JOURNAL OF AUTOIMMUNITY, 2000, 14 (01) :63-78