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. 2021 Apr 1;8:662047. doi: 10.3389/fmolb.2021.662047

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Copyright © 2021 Carvalho and Hedrich.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Psoriatic arthritis is a multifactor disease. Dendritic cells (DC) play a central role in the pathogenesis of psoriatic arthritis. DC activated by different stimuli produce and secrete IL-23 and IL-12 which further stimulate Th17, γδT cells and ILC3 and Th1 cells, respectively, leading to the production of inflammatory cytokines. Inflammatory cytokines can act by activating the JAK/STAT signaling pathway which regulates the expression of RANKL. RANKL binds to RANK activating osteoclast precursors. Environmental triggers such as changes in the microbiota, PAMPs (pathogen associated molecular patterns), and LPS can trigger the development of inflammatory cascades such as the MyD88/IRAK/TRAF6 pathway. Epigenetic mechanism, namely non-coding RNAs (e.g., MiR-146a), has been suggested as a critical link between environmental triggers and aberrant inflammatory responses. PsA genetic associations are highlighted with a red *.