Abstract
Psoriatic arthritis (PsA) is a complex immune-mediated disease and its pathogenesis depends both on genetic factors and environment. PsA patients may present a wide range of clinical manifestations including skin and nail abnormalities. Indeed, articular involvement is variable too. Disease development relies on a heterogeneous net made of multiple cytokines pathways which are regulated by several factors including human leucocyte antigen (HLA) expression, miRNAs, microbiome. Among genetic polymorphisms which can lead to abnormal cytokine expression, tumor necrosis factor (TNF) polymorphisms have been studied. Thus, leading to the development of new therapeutic agents. Finally, further studies on genetic factors and epigenetics will give new insights into this complex disorder. The aim of this mini-review is to provide the reader with a summary of the fundamental and most innovative aspects of genetic and epigenetic factors involved in the PsA, thus including human leucocyte antigen (HLA) expression, tumor necrosis factor (TNF) polymorphisms, micro RNAs and microbiome.
Highlights
Psoriatic arthritis (PsA) is a complex immune-mediated disease which occurs in 30% of patients suffering from psoriasis [1]
Disease development relies on a heterogeneous net made of multiple cytokines pathways which are regulated by several factors including human leucocyte antigen (HLA) expression, miRNAs, microbiome
Among genetic polymorphisms which can lead to abnormal cytokine expression, tumor necrosis factor (TNF) polymorphisms have been studied
Summary
Psoriatic arthritis (PsA) is a complex immune-mediated disease which occurs in 30% of patients suffering from psoriasis [1]. Considering the different timing of articular and skin involvement, a multidisciplinary approach is essential to avoid diagnosis delay. Diagnostic criteria for PsA have not been validated, but the Classification Criteria for PsA (CASPAR criteria), published in 2006, define psoriatic arthritis for the purpose of enrolling patients in clinical trials and provide guidance to clinicians [1]. Recent studies on regulatory lymphocytes demonstrated that CD8+ T suppressor (Ts) cells may have great relevance in controlling immune system homeostasis and avoiding the development of chronic inflammatory immune-mediated diseases. It has been reported that type 2 CD8+ Ts cells may be involved in the control of pathologic chronic immune responses, contributing in some cases to the pathogenesis of the inflammatory immune-mediated diseases including PsA [5]. New agents as anti-TNF agents, including etanercept, infliximab, adalimumab, golimumab and certolizumab, as well as the newest molecules as oral phosphodiesterase 4 inhibitor (apremilast), Janus kinase (JAK) inhibitor (tofacitinib) and anti-IL-23/IL-17 pathway including secukinumab, brodalumab, ixekizumab, and ustekinumab have been developed
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