Abstract
Transcriptome profiling approaches have been widely used to investigate the mechanisms underlying psoriasis pathogenesis. Most researchers have measured changes in transcript abundance in skin biopsies; relatively few have examined transcriptome changes in the blood. Although less relevant to the study of psoriasis pathogenesis, blood transcriptome profiles can be readily compared across various diseases. Here, we used a pre-established set of 382 transcriptional modules as a common framework to compare changes in blood transcript abundance in two independent public psoriasis datasets. We then compared the resulting “transcriptional fingerprints” to those obtained for a reference set of 16 pathological or physiological states. The perturbations in blood transcript abundance in psoriasis were relatively subtle compared to the changes we observed in other autoimmune and auto-inflammatory diseases. However, we did observe a consistent pattern of changes for a set of modules associated with neutrophil activation and inflammation; interestingly, this pattern resembled that observed in patients with Kawasaki disease. This similarity between the blood-transcriptome signatures in psoriasis and Kawasaki disease suggests that the immune mechanisms driving their pathogenesis might be partially shared.
Highlights
Inflammation has an important role to play as part of the host defense against infection
Such information can be obtained via blood transcriptome profiling, whereby all RNA species that are present in a given sample are measured simultaneously
Vast amounts of blood transcriptome profiling data are available in public repositories that can be used for contextual interpretation and “benchmarking” of blood transcriptional signatures
Summary
Inflammation has an important role to play as part of the host defense against infection. Current treatment modalities include topical glucocorticoids, vitamin D analogues, phototherapy, conventional immunosuppressives (e.g., ciclosporin, methotrexate), and various biologics that target TNF-a (e.g., infliximab), the IL-17 pathway (e.g., secukinumab), and IL12/IL-23 (e.g., ustekinumab) [9,10,11,12]. Despite such progress in understanding the molecular mechanisms driving psoriasis, we are still far from having a complete understanding of the immunopathogenesis and developing highly effective therapeutics
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