REPORT

Psoriatic arthritis and psoriasis: classification, clinical features, pathophysiology, immunology, genetics

Immunopathology of psoriasis and psoriatic arthritis

D J Veale¹, C Ritchlin², O FitzGerald¹

¹ St Vincent’s University, Dublin, Ireland
² University of Rochester Medical School, Rochester, NY, USA

Correspondence to:
Correspondence to:
Dr D J Veale
Department of Rheumatology, St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland; d.veale{at}st-vincents.ie

Psoriatic arthritis (PsA) is characterised by several unique clinical features that differentiate it from rheumatoid arthritis (RA). Attempts to identify immunopathological mechanisms, some shared with psoriasis, that underlie these differences from RA have been most challenging. Recent research studies, however, highlight novel findings in PsA at the molecular, cellular, and tissue levels that form the basis for a new understanding of this relatively common form of inflammatory arthritis. In particular, the availability of new, biological antitumour necrosis factor therapies have allowed further insight into the immunopathology of psoriasis and PsA. This brief review focuses on immunohistological studies in psoriatic skin, PsA synovium, and bone to demonstrate how these data advance our knowledge of disease pathogenesis.

Abbreviations: APC, antigen presenting cell; CLA, cutaneous lymphocyte associated antigen; HLA, human leucocyte antigen; ICAM, intercellular adhesion molecule; IL, interleukin; MHC, major histocompatibility complex; MMP, matrix metalloproteinase; NKR, natural killer receptor (cell); PsA, psoriatic arthritis; RA, rheumatoid arthritis; RANK(L), receptor activator of nuclear factor B (ligand); TCR, T cell receptor; TGF, transforming growth factor; TNF, tumour necrosis factor; VEGF, vascular endothelial growth factor; VCAM, vascular cell adhesion molecule

Keywords: TNF; immunohistology; pathogenesis; psoriasis; psoriatic arthritis

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