Researchers identified 125 independent susceptibility loci linked to psoriasis, including 17 previously unreported loci, according to a peer-reviewed study published in Nature Communications on August 27, 2026. The investigators performed a large-scale genome-wide meta-analysis across 1,131,685 individuals of European ancestry to examine the genetic architecture of the heritable chronic autoimmune disorder.
Combining genomic findings with single-cell transcriptomic data revealed predominant roles for myeloid and T cells in psoriasis. The joint analysis also identified enriched expression of disease-associated genes within keratinocytes and endothelial cell subsets.
Applying multiple robust approaches, the research team prioritized 50 potential therapeutic target genes. The authors mapped cell subtype-specific activity patterns for these targets across non-lesional, lesional, and treatment conditions. Those activity patterns revealed layer-specific cross-cell-type interactions and highlighted the role of immunometabolism in disease progression.
Data access for the research included analysis approved under UK Biobank Application Number 33002, alongside contributions from research participants and employees of 23andMe, Inc. The work received grant funding from the National Research Foundation of Korea through awards RS-2022-NR070328 and RS-2023-00223277, supported by the Korean Ministry of Science and ICT.
The paper lists authors from several institutions, including Sungkyunkwan University, Kyung Hee University College of Medicine, Boston Children’s Hospital, Mass General Brigham, Harvard Medical School, and the Broad Institute of MIT and Harvard. Nature Communications received the original submission on May 30, 2025, and formally accepted the paper on August 17, 2026. Study co-author Woong-Yang Park is employed by GENINUS in a role unrelated to the research, while the remaining contributors reported no competing interests.
