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Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and ‘Type 1’ inflammatory gene expression

2004; Elsevier BV; Volume: 25; Issue: 6 Linguagem: Inglês

10.1016/j.it.2004.03.006

1471-4981

Wook Lew, A. Bowcock, James G. Krueger,

T-cell and B-cell Immunology

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-γ (IFN-γ) 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-3β (MIP-3β; 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.