title: Etiology and Pathogenesis of Psoriatic Arthritis.
abstract: The current model of psoriatic arthritis implicates both the IL-23/IL-17 axis and the tumor necrosis factor (TNF) pathways in disease pathogenesis. Although specific major histocompatibility complex class I molecules are associated with the psoriatic disease phenotype, no specific antigen or autoantibody has been identified. Instead, an array of genes may code for an autoinflammatory loop, potentially activated by mechanical stress and dysbiosis in the skin or gut. Danger signals released by innate immune cells activate a Th1 and Th17 response that leads to synovitis, enthesitis, axial inflammation, and altered bone homeostasis characterized by pathologic bone resorption and new bone formation.
authors.affiliation: Allergy, Immunology and Rheumatology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 695, Rochester, NY 14642, USA.
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Barnas
authors.affiliation: Allergy, Immunology and Rheumatology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 695, Rochester, NY 14642, USA. Electronic address: Christopher_Ritchlin@urmc.rochester.edu.
authors.forename: Christopher T
authors.initials: CT
authors.lastname: Ritchlin
mesh_terms: D015535:Arthritis, Psoriatic / Q000209:etiology / Q000235:genetics / Q000276:immunology; D004781:Environmental Exposure / Q000009:adverse effects*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate; D012307:Risk Factors
keywords: Dactylitis; Enthesitis; IL-17; IL-23; Inflammatory arthritis; Psoriasis; Psoriatic arthritis; Spondyloarthropathy