AI Summary
A recent study found that blocking interleukin-17A can effectively treat psoriasis by suppressing autoimmune functions and reducing symptoms. This approach shows promise for developing a cure for psoriasis, a chronic autoimmune skin condition.
In a recent study published in the journal Frontiers in Immunology, researchers use a multi-omics approach combining immune cell-enriched single-cell transcriptomics (scRNA-seq), microarray analysis, and immunohistochemistry to elucidate the translational role of anti-interleukin-17A (IL-17A) in suppressing the autoimmune functions of type 17 T-cells (T17), thereby effectively treating human psoriasis.
Study: Multi-omics segregate different transcriptomic impacts of anti-IL-17A blockade on type 17 T-cells and regulatory immune cells in psoriasis skin. Image Credit: Anatolev/Shutterstock.com
Their results show that systemic IL-17A blockade depleted almost all IL17A+ and IL17F+ T-cells and caused significant downregulations in interleukin-23A (IL23A) gene expression, causing long-term reduction in psoriasis symptoms, even after medication has been halted. The IL-17A blockade was also found to upregulate CD1C and CD14 gene expression. Together, these results highlight the benefits of biologics blocking the IL-23/Type 17 T-cell autoimmune axis, with the potential for novel monoclonal antibodies that might finally present a cure for psoriasis, a hitherto uncurable condition.
Psoriasis
Psoriasis is a non-communicable, autoimmune skin condition characterized by scaly and itchy rashes that most commonly present on affected patients’ scalp, trunk, elbows, and knees. It is generally a chronic, life-long disease, and while topical treatments have been proven effective in symptomatically treating mild- to moderate disease manifestations, a lasting cure for the disease remains elusive.
Psoriasis is one of the most common autoimmune disorders in humans, with over 3.2% of all people estimated to be afflicted. While not directly lethal, psoriasis presents comorbidities, including metabolic abnormalities, psoriatic arthritis, overt vascular inflammation,