Genetic and inflammatory factors associated with psoriatic arthritis: Relevance to diagnosis and management

Pathogenesis of psoriasis in the “omic” era. Part IV. Epidemiology, genetics, immunopathogenesis, clinical manifestation and treatment of psoriatic arthritis

“…Genetic predisposition together with environmental triggers, in which gut dysbiosis favors the ingenerating tissue damage by damage-associated-molecular-patterns (DAMPs), induce release of pathogen-associated-molecular-patterns (PAMPs), or repetitive entheseal mechanical stress production of inflammatory infiltrates consisting of monocytes, dendritic cells (DCs), other antigen presenting cells (APCs), neutrophils as well as T cells in the enthesis and synovium [ 26 , 27 ] ( Figure 1 ). Pathogenesis of psoriatic arthritis (PsA) starts with activation of the innate immune system cells, i.e.…”

“…Entheseal resident macrophages, NK cells and T cells, retinoic acid-related orphan receptor-gamma t(ROR-γt+) CD3+CD4-CD8-IL-23R+ T cells are activated by IL-23 produced by DCs [ 36 ]. The entheseal resident cells and other innate immune cells are regarded as the main sources of IL-6, IL-17, IL-22 and chemokines (C-X-C motif ligand 1) [ 27 , 30 ]. The resident γδ T cells and type 3 innate lymphoid cells (ILCs) release cytokines, i.e.…”

“…The TNF-α inhibitors may reduce the infiltration of T cells and macrophages in the synovium, they are also capable of decreasing the Th17 level in the synovial fluid and then cause theTh17 outflow from the synovium into the lymph nodes and bloodstream. They also reduce the level of circulating OCPs in the patients with erosive PsA [ 27 , 37 ]. In the developed PsA, the TNF inhibitors slow down the progression of structural joint damage and reduce bone resorption, but they do not prevent new bone formation [ 41 ].…”

Longitudinal profiling of the gut microbiome in patients with psoriatic arthritis and ankylosing spondylitis: a multicentre, prospective, observational study

“…The pathogenesis of the disease is poorly understood however there is evidence of a genetic component in PsA, it has been demonstrated by studies showing an increased recurrence in first degree relatives [6]. Genes that have been demonstrated associated with an increased risk of developing psoriatic arthritis include HLA-B27, IL 13 and PTPN22, with the strongest association demonstrated for HLA B27 [7]. HLA-B27 is a well-established major risk factor for the development of ankylosing spondylitis (AS), but also 15-20% of PsA patients express HLA-B27 with a stronger association with the axial distribution of the disease [8,9].…”