Pathogenesis of Psoriatic arthritis

Pathogenesis of Psoriatic arthritis

It is thought that PsA begins as a complex interaction of genetic and environmental factors.

When skin disease precedes arthritis, inflammation in the skin damages keratinocytes and releases their DNA, leading to triggering of interferon gamma.

This activates dermal dendritic cells which migrate to local lymph nodes. There, TH1 and TH17 cells differentiate and proliferate.

When these cells return to the dermis, they release IL-12, IL-17, IL-22, TNFα, and inflammatory cytokines that perpetuate the cycle of tissue damage and inflammation.

CD8+ T cells are also thought to be important. CD8+ and CD4+ T cells are higher in number in the synovial fluid of patients with PsA than in those with RA.

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