Multi-omics approach identifies PI3 as a biomarker for disease severity and hyper-keratinization in psoriasis.

Background: Psoriasis is an immune-mediated inflammatory skin disease. Psoriasis severity evaluation is important for clinicians in the assessment of disease severity and subsequent clinical decision making. However, no objective biomarker is available for accurately evaluating disease severity in psoriasis.

Longitudinal Follow-Up Using the Heel Enthesitis Magnetic Resonance Imaging Scoring System (HEMRIS) Shows Minimal Changes in Heel Enthesitis Assessed in Spondyloarthritis and Psoriasis Patients.

Enthesitis is a common clinical feature of spondyloarthritis (SpA). For reliable assessment of enthesitis the Heel Enthesitis Magnetic Resonance Imaging Scoring System (HEMRIS) was developed. The aims of this study were to evaluate changes in HEMRIS over time and to evaluate whether these changes correlated with changes in clinical parameters.

Multi-omics integration reveals a core network involved in host defence and hyperkeratinization in psoriasis.

Objectives: The precise pathogenesis of psoriasis remains incompletely explored. We aimed to better understand the underlying mechanisms of psoriasis, using a systems biology approach based on transcriptomics and microbiome profiling.

Methods: We collected the skin tissue biopsies and swabs in both lesional and non-lesional skin of 13 patients with psoriasis, 15 patients with psoriatic arthritis and healthy skin from 12 patients with ankylosing spondylitis.

Regulatory T cells in psoriatic arthritis: an IL-17A-producing, Foxp3CD161 + RORγt + ICOS + phenotype, that associates with the presence of ADAMTSL5 autoantibodies.

In psoriatic arthritis (PsA), predisposing class I HLA alleles, the presence of synovial clonally proliferated CD8 + T cells and autoantibodies all point towards the loss of immune tolerance. However, the key mechanisms that lead to immune dysregulation are not fully understood. In other types of inflammatory arthritis, T regulatory cell (Treg) dysfunction and plasticity at sites of inflammation were suggested to negatively affect peripheral tolerance.