In a recent article published in the journal Frontiers in Immunology, researchers across Europe investigated deoxyribonucleic acid (DNA) methylation patterns in the cluster of differentiation (CD)4+ T-cells from psoriasis and psoriatic arthritis (PsA) patients as these might represent potential biomarkers of psoriasis/PsA.
Study: DNA methylation patterns in CD4+ T-cells separate psoriasis patients from healthy controls, and skin psoriasis from psoriatic arthritis. Image Credit: And-One / Shutterstock
Background
Studies have identified ~3,000 differentially methylated positions (DMPs) in psoriasis and PsA patients. Typically, chronic joint inflammation triggering PsA manifests within 10 years after the onset of skin psoriasis; however, in nearly 15% of patients, PsA is the initial presentation, which leads to diagnostic delays.
Even though the complex pathophysiology of psoriasis/PsA remains incompletely understood, studies have established the role of epigenetic dysregulation involving effector CD4+ and CD8+ T-cells and the tumor necrosis factor (TNF)/interleukin (IL-)23/IL-17 cytokine axis in their pathophysiology.
It is a key pathway in all T-cell-mediated chronic autoimmune/inflammatory diseases, including psoriasis and PsA. T helper 17 (Th17) cells are a unique Th-cell subset known to secrete IL-17 and other key inflammatory effector cytokines involved in psoriasis. IL-23 promotes the survival and maintenance of Th17 cells; accordingly, researchers have observed its higher expression in psoriatic skin lesions.
Studies have also shown that the blockade of IL-17/23 is an effective treatment for psoriasis/PsA. Likewise, a recently identified Th22 effector Th-cell cell subset, characterized by IL-22/13 production, has been implicated in psoriasis.
Overall, therapeutic interventions targeted at correcting altered DNA methylation patterns in psoriasis/PsA might help permanently resolve