The differential effects reported here for the above-mentioned treatment modalities could be exploited to optimize or design therapeutic strategies to overcome the inflammatory drivers more effectively and restore the Th17-Treg balance in psoriasis.
Summary
Psoriasis is a common condition that affects the skin and joints. Skin psoriasis tends to wax and wane throughout life without obvious reasons, and thus causes considerable distress. Someone with psoriasis may have other family members with the same problem but this is not usually the case. In psoriasis, more skin cells are made leading to build‐up on the top layer and formation of flaky patches on the skin or severe dandruff of the scalp. The cause is unknown and believed to involve the genes and immune system, and the treatments we use now can control psoriasis but don't cure it. This study from Aberdeen, UK looked into two types of cells of the immune system; one of them can start or cause psoriasis to happen, while the other has the power to fight back and calm down the skin. We tested the effect of certain injections, cream and light which we frequently use to treat psoriasis, on those cells by taking blood and skin samples. We found that the skin became better after six weeks. The light made the numbers of the “good” cells go higher, while the injection caused the “bad” cells to become fewer and had no effect on the “good” cells. The cream increased the “good” cells and reduced the “bad” cells. We noticed these changes in both the blood and skin which means that the cream and light can have an effect on cells in the circulation and this can be used in the future to make new and safer treatments.
Identifying differential expression of genes in psoriatic and healthy skin by microarray data analysis is a key approach to understand the pathogenesis of psoriasis. Analysis of more than one dataset to identify genes commonly upregulated reduces the likelihood of false positives and narrows down the possible signature genes. Genes controlling the critical balance between T helper 17 and regulatory T cells are of special interest in psoriasis. Our objectives were to identify genes that are consistently upregulated in lesional skin from three published microarray datasets. We carried out a reanalysis of gene expression data extracted from three experiments on samples from psoriatic and nonlesional skin using the same stringency threshold and software and further compared the expression levels of 92 genes related to the T helper 17 and regulatory T cell signaling pathways. We found 73 probe sets representing 57 genes commonly upregulated in lesional skin from all datasets. These included 26 probe sets representing 20 genes that have no previous link to the etiopathogenesis of psoriasis. These genes may represent novel therapeutic targets and surely need more rigorous experimental testing to be validated. Our analysis also identified 12 of 92 genes known to be related to the T helper 17 and regulatory T cell signaling pathways, and these were found to be differentially expressed in the lesional skin samples.
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