Etiology and Pathogenesis of Psoriatic Arthritis

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 autoant...

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Bibliographic Details
Published inRheumatic diseases clinics of North America Vol. 41; no. 4; p. 643
Main Authors Barnas, Jennifer L, Ritchlin, Christopher T
Format Journal Article
LanguageEnglish
Published United States 01.11.2015
Subjects
Arthritis, Psoriatic - etiology
Arthritis, Psoriatic - genetics
Arthritis, Psoriatic - immunology
Environmental Exposure - adverse effects
Genetic Predisposition to Disease
Humans
Immunity, Innate
Risk Factors
Dactylitis
Enthesitis
Spondyloarthropathy
Psoriasis
Inflammatory arthritis
IL-17
IL-23
Psoriatic arthritis
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Summary: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.
ISSN:1558-3163
DOI:10.1016/j.rdc.2015.07.006