Psoriasis may cause the repositioning of immune cells into the upper layers of the skin as the disease progresses, according to a new study published by Castillo et al in Science Immunology. Researchers integrated spatial transcriptomics with publicly available single-cell transcriptomics data to profile the skin biopsies of 25 patients who either did not have psoriasis or had psoriasis—including those with or without lesional skin and with or without psoriatic arthritis—with the goal of better understanding the differences in immune cell distribution in individuals with inflamed vs healthy skin. The researchers discovered that patients who had skin lesions presented with inflammation in the outer and inner layers of the skin and B cells in the upper layers of the skin, whereas patients who did not have psoriasis had no B cells in the skin. Further, by identifying genetic activity as well as the location of fibroblasts within the skin biopsies, the researchers were able to differentiate between patients with mild disease who had fibroblasts in the upper skin layers and those with moderate to severe disease who had fibroblasts deeper in the skin and higher levels of gene signatures associated with metabolic dysfunction. However, the researchers were unable to tell the differences between those with and without psoriatic arthritis. In a companion press release from the National Institutes of Health, the study authors concluded that spatial transcriptomics may have successfully “[offered] the most comprehensive archive of cellular and molecular features involved in both diseased and healthy skin.” The researchers hope their new findings can help illuminate how skin inflammation can result in extracutaneous manifestations.
June 30, 2023