Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment

Version 1 : Received: 27 June 2023 / Approved: 28 June 2023 / Online: 28 June 2023 (12:30:45 CEST)

A peer-reviewed article of this Preprint also exists.

Lee, B.-W.; Moon, S.-J. Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment. Int. J. Mol. Sci. 2023, 24, 11662. Lee, B.-W.; Moon, S.-J. Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment. Int. J. Mol. Sci. 2023, 24, 11662.

Abstract

Psoriatic arthritis (PsA) is a persistent, inflammatory disease that affects individuals with psoriasis, arthritis, and enthesitis. Research has demonstrated that inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-23 (IL-23), and interleukin-17 (IL-17) play a pivotal role in both the onset and progression of PsA. These cytokines are generated by activated immune cells and stimulate the attraction of inflammatory cells to the synovium and joint tissues, resulting in the deterioration of cartilage and bone. The blocking of these cytokines has become a successful treatment strategy for PsA, as biological drugs that inhibit TNF-α, IL-23, and IL-17 have demonstrated notable clinical benefits. The association between PsA and other types of inflammatory cytokines or chemokines, excluding TNF-α, IL-23, and IL-17, has been extensively investigated in numerous studies. These findings may provide a chance for the discovery of novel therapeutic agents targeting other molecules, distinct from the currently approved biologics and targeted synthetic disease-modifying antirheumatic drugs. In this review, we discuss the current understanding of the role of inflammatory cytokines in PsA pathogenesis and clinical implications of targeting these cytokines for PsA treatment.

Keywords

psoriatic arthritis; inflammatory cytokines; tumor necrosis factor-alpha; interleukin-17; interleukin-23; JAK/STAT signaling pathway

Subject

Biology and Life Sciences, Immunology and Microbiology

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