Journal
TRENDS IN IMMUNOLOGY
Volume 25, Issue 6, Pages 295-305Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2004.03.006
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Funding
- NCRR NIH HHS [M01 RR 00102] Funding Source: Medline
- NIAID NIH HHS [AI 49832, AI 14957 2] Funding Source: Medline
- NIAMS NIH HHS [R01 AR 49049] Funding Source: Medline
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Psoriasis vulgaris is a common inflammatory skin disease that involves infiltration of leukocytes, activation of skin-resident cells and increased production of numerous cytokines, chemokines and inflammatory molecules. This Review presents an integrated view of disease pathogenesis, taking into account immune biology, broad-scale genomic characterization and the response of psoriasis to immune-targeted therapies. Recent studies suggest that activated dendritic cells (DCs) and T cells are central to its pathogenesis, causing 'inflammation' through a pathway of sequential interleukin-23 (IL-23) synthesis, interferon-gamma (IFN-gamma) production, activation of STAT1 (signal transducer and activator of transcription 1) and subsequent transcription of a broad series of IFN- and STAT-1-regulated genes. In situ expression of macrophage inflammatory protein-3beta (MIP-3beta; CCL19), secondary lymphoid tissue chemokine (SLC; CCL21) and other chemokines normally confined to formal lymphoid tissues, might help to sustain DC accumulation and overall activation of this inflammatory pathway.
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