Psoriatic arthritis (PsA) is a chronic inflammatory skin disease that causes enthesitis and destructive arthritis and significantly lowers patient quality of life. Recognition of the two target organs (the skin and joints) involved in the immunopathophysiology of PsA helped in elucidating the pathology of various systemic autoimmune diseases targeting multiple organs. Recent advances in immunology and genetics have made it clear that acquired immunity, especially that mediated by the Th17/IL-23 axis, plays an important role in the inflammatory pathology observed in psoriasis and PsA. Additionally, involvement of natural immunity has also been suggested. Microbial infection has been known to trigger psoriasis and PsA. Recent clinical studies using biopharmaceuticals, such as tumor-necrosis-factor- (TNF-) α inhibitors and IL-12/23 p40 antibodies, indicate that studies need not be based only on the immunological phenomena observed in PsA pathology since disease pathology can now be verified using human-based science. Considering this aspect, this paper discusses the immunopathology of PsA compared to psoriasis (cutaneous) and rheumatoid arthritis in humans and immunopathology of PsA with respect to the Th17/IL-23 axis and microbial infection. 1. Introduction Psoriasis is a typical inflammatory keratosis, characterized by inflammation, telangiectasia, hyperproliferation, and abnormal differentiation of epidermal cells, and it is sometimes complicated by arthritis. There is considerable variation in reports concerning the transition from psoriasis to psoriatic arthritis (PsA), with figures ranging from 6% to 42%. The onset of cutaneous psoriatic eruptions usually precedes that of PsA; a study involving 1000 patients with PsA showed that cutaneous eruptions preceded the onset of PsA in 86% of cases by more than 12 years [1, 2]. PsA often causes destructive arthritis and arthropathy, which considerably decrease patient quality of life. Thus, clinicians must anticipate when patients with psoriasis vulgaris will progress to arthropathic psoriasis and intervene decisively in the early stages of onset of arthropathy, therapeutically targeting psoriatic skin and joint inflammation. Psoriasis can affect two target organs—the skin and synovial membrane—and its main pathogenesis is considered to be chronic inflammation. The cause of this disease is probably based on the common foundations of autoimmune or autoinflammatory pathology. The mechanism by which this occurs begins with antigen-presenting cells, which are presumed to activate cutaneous and synovial membrane T
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