Psoriasis: pathogenesis, progression, and treatment
OA Version
Citation
Abstract
Psoriasis (PsO) is a chronic, immune-mediated skin disease that arises from a complex interplay of genetic predisposition, environmental triggers, and immune dysregulation. Early-onset PsO is associated with familial inheritance and specific loci such as HLA-Cw6, along with polymorphisms in genes linked to the IL-23/Th17 axis. Environmental factors that take the form of infections, physical trauma, air pollution and stress can trigger or exacerbate flares. A dysregulated immune system, including abnormal keratinocytes and dendritic cell and T cell interactions, drives psoriatic inflammation via cytokines and intracellular pathways such as NF-κB. Treatment approaches can look like traditional topicals to targeted biologics and novel delivery systems. First-line topical agents like vitamin D analogs, corticosteroids, retinoids, calcineurin inhibitors, and emollients effectively address mild to moderate PsO, often as combination therapies. Phototherapy, specifically narrowband UVB, has shown to be an important adjunct or alternative. Systemic treatments like methotrexate and cyclosporine have spurred the development of biologics: TNF-α inhibitors and IL-12/23, IL-17, and IL-23 inhibitors. These induce better skin clearance with lower toxicity. Nanofiber formulations and microneedle patches are additional new developments that seek to enhance drug penetration and minimize side effects. Attention has also turned to modifiable lifestyle factors, as weight management and anti-inflammatory diets may mitigate PsO symptoms. Additionally, treating gut and skin dysbiosis with probiotics or fecal microbiota transplantation is continually being explored. By integrating pharmacologic treatments, innovative drug delivery, and holistic care, PsO treatment can become individualized with patients seeing sustained remission and improved quality of life.
Description
2025