© 2005 by BMJ Publishing Group Ltd & European League Against Rheumatism
REPORT
Psoriatic arthritis and psoriasis: classification, clinical features, pathophysiology, immunology, genetics
Psoriasis pathophysiology: current concepts of pathogenesis
1 Laboratory for Investigative Dermatology, Rockefeller University, New York, USA
2 Department of Genetics, Washington University School of Medicine, St. Louis, MO, USA
Correspondence to:
Correspondence to:
J Krueger
Rockefeller University, 1230 York Ave, New York, NY 10021 USA; jgk{at}rockefeller.edu
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 epithelial 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 leucocyte 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 target T cells have 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.
Abbreviations: CLA, cutaneous lymphocyte antigen; iDC, immature dendritic cell; IFN, interferon; IL, interleukin; LFA-1, leucocyte function associated antigen-1; mDC, mature dendritic cell; MHC, major histocompatibility complex; NF
B, nuclear factor
B; NK-T, natural killer T (cells); pDC, plasmacytoid dendritic cell; PsA, psoriatic arthritis; RA, rheumatoid arthritis; STAT, signal transducer and activator of transcription; TNF, tumour necrosis factor; TCR, T cell receptor; TOR, target of rapamycin
Keywords: PSORS2; T cells; dendsitic cells; gene expression or genomics; psoriasis genes or genetics
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