Psoriasis is a chronic, complex, inflammatory autoimmune disease that causes the rapid accumulation of skin cells (epidermal keratinocytes). It affects 2 to 3% of the population and the disorder frequently occurs in 5 to 10% of patients. Factors such as genetics and environment contribute to the risk of becoming infected with psoriasis (Constantinides et al., 2014). Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay This accumulation of cells causes flaking on the surface of the skin. Inflammation and redness around the scales are quite common. Typical psoriatic scales are whitish-silver and develop into thick, red patches. Sometimes these patches crack and bleed. Psoriasis is the result of an accelerated skin production process. Typically, skin cells grow deep in the skin and slowly rise to the surface. Eventually, they fall. The typical life cycle of a skin cell is one month. Scalp psoriasis is a common skin disease that causes mild, intermittent, scaly, red, patchy lesions to form on the scalp until the scalp is completely involved. It may appear as one or more patches, and may even affect your entire scalp. It can also spread to your forehead, the back of your neck, or behind and inside your ears. There may be a link between skin patches and joint pain, which are some of the signs and symptoms of psoriatic arthritis, a condition that may be linked to psoriasis. The symptoms of psoriasis differ from person to person and depend on the type of psoriasis. Areas of psoriasis can be as small as a few flakes on the scalp or elbow or cover the majority of the body. The most common symptoms of plaque psoriasis include: red, inflamed patches of skin, silvery-white scales or patches over the red patches, dry skin that may crack and bleed, pain around the patches, itching and soreness. burning sensations around the plates, thick and pitted nails. swollen and painful joints. In a recent study, genetic variances were noted between normal and skin psoriasis cells compared to scalp psoriasis. They found similarities in the gene expression of many immunological molecules. In the scalp, the most upregulated LS genes in scalp LS include S100A12, DEFB4, IL1F9 (encoding IL-36?), and IL8 (all >20-fold higher than scalp NL) and all genes regulated by IL-17, such as OASL, KYN4, PI3, CCL20, S100A9, LCN2, CXCL9, IFI27, and OAS1. In gene comparisons, we found that psoriasis background NL scalp had intermediate gene expressions between LS and N scalp, implying low levels of inflammation in this tissue. In cutaneous psoriasis, many other genes are highly represented in the skin transcriptome. Differences were found in LCN2, KRT6 are all significantly upregulated in psoriasis vulgaris LS. These genes, which show constitutively high expression in NL and N scalp biopsies, are upregulated to a lesser extent in LS scalp biopsies. In contrast, scalp tissues showed lower expression of CD1A and CD207/langerin (groups 2 and 3), which are markers of LCs. The LCN2 gene encodes lipocalin-2, a protein involved in innate immunity that sequesters iron and therefore limits bacterial growth. Therelipocalin-2 is expressed in neutrophils, monocytes and keratinocytes; its serum levels are increased in patients with psoriasis and correlate with disease severity. KLK6 encodes a serine protease with activity against extracellular matrix proteins, such as fibronectin, laminin, vitronectin, and collagen, and is elevated in both PsA synovial fluid and psoriatic plaques. Thus, genes induced by TNFa, IL-17, IL-22, interferons and other inflammatory cytokines are generally very similar in scalp and skin psoriasis. However, normalized GSEA enrichment scores of all genes in the disease transcriptome were slightly higher in cutaneous LS than in scalp LS, a finding that may be explained by constitutive expression of some genes of the psoriatic transcriptome in the follicular epithelium of the NL.scalp. To estimate variations in pathway activity in scalp psoriasis transcriptomes, we performed GSVA. Scalp transcriptomes were particularly enriched in “basal vs upper epidermis”, “melanocytes”, “fibroblasts” and “CD4+ T cells” and INF-activated keratinocyte profiles? or IL-13 and myeloid DCs induced by IL-17. Interestingly, enrichment of “negative regulators” and “epigenetically regulated psoriasis-related genes” was also observed. Skin transcriptomes were associated with significant enrichment of gene sets related to “epidermal differentiation complex”, “cornified envelope”, “keratinocytes”, “T lymphocytes”, “PBMC”, “ macrophages”, to “mature DC”, to “immature DC”. ', 'Th17', 'Th22' and gene sets related to TNFa/IL-17/IL-22-induced keratinocyte responses. When comparing immune gene sets by GSEA, scalp psoriasis resembles cutaneous psoriasis and, to a much lesser extent, mouse models. STAT3, Tie2 and TGF? The transgenic models and the imiquimod-induced model represent mouse models that express some inflammatory pathways present in psoriasis vulgaris, but with lower fidelity in the range of pathways expressed in the human disease. In our case, the IL-23-induced mouse transcriptome showed the greatest resemblance to human skin and scalp psoriasis. Although the scalp is considered closer to the skin in animal models, psoriasis remains an IFL skin disease even at the scalp level. To validate the microarray results, we performed RT-PCR. Expression of IFN-?, IL-23p19, IL-12/23p40, IL-17, and IL-22 was higher in scalp psoriasis samples LS than in NL scalp psoriasis samples, as previously described for LS psoriasis. We also analyzed mRNA for IL-20, a cytokine produced by inflammatory dendritic cells (iDCs) that affect keratinocyte activation and proliferation and found it to be significantly higher in leather samples. hairy LS than in NL. Higher mRNA expression of iNOS, an inducible nitric oxide synthase produced by Tip-DCs, was also observed in scalp LS, similar to previous reports in cutaneous psoriasis. We also analyzed the immune phenotypic profiles of scalp and skin psoriasis in relation to AA and AD. Scalp psoriasis showed a Th1/Th17 activation profile, similar to cutaneous psoriasis, but with more Th1 activation and less Th22 activation. We also found.