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We read with great interest the article by Gao et al.1 They have reported the regulatory role of the JAK/STAT kinase system on the inflammatory/proliferative cascades for pannus formation in psoriatic arthritis (PsA) such as on fibroblast like synovial cells (FLS) biology and on secretion of inflammatory cytokines (interleukin (IL) 6, IL-8, monocyte chemoattractant protein (MCP)-1) by these FLS. Tofacitinib targets JAK1 and JAK2 with IC50 values in the same order of magnitude as that of JAK3.2 They have also provided the mechanisms of actions of tofacitinib by demonstrating that tofacitinib significantly decreased pSTAT3, pSTAT1, NFκBp65 in PsAFLS and inhibits the cellular and molecular events of pannus formation. However, Gao et al did not address a critical issue whether JAK/STAT signalling system regulates the IL-23/IL-17 cytokine axis in PsA. Here we are sharing an alternative mechanism for the role of JAK/STAT kinase system in the pathogenesis of PsA.
Aberrant activation of IL-23/IL-17 cytokine axis is a dominant pathology in PsA. …
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