Psoriasis is a chronic, complex, inflammatory, autoimmune condition that causes the rapid accumulation of skin cells (epidermal keratinocytes). It affects 2-3% of the population and involvement occurs frequently in 5-10% of patients. Factors such as genetics and environmental factors contribute to the risk of contracting psoriasis (Constantinides et al., 2014). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay This buildup of cells causes flaking on the surface of the skin. Inflammation and redness around the scales are quite common. Typical psoriatic scales are silver-white in color 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 into 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 involves the formation of mild, intermittent, scaly, red, bumpy lesions on the scalp up to total scalp involvement. It can appear as a single patch or several and can even affect the entire scalp. It can also spread to the forehead, back of the neck, or behind and inside the ears. There may be a connection between skin plaques and joint pain which are some of the signs and symptoms of psoriatic arthritis, a condition that can be related 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 most of the body. The most common symptoms of plaque psoriasis include: red, inflamed patches of skin, silver-white scales or plaques on the red patches, dry skin that may crack and bleed, pain around the patches, itching and burning sensations around the patches, nails thick and pitted, joints swollen and painful. In a recent study, genetic variations were noted between normal and skin psoriatic cells compared to scalp psoriasis. Similarities have been found in the gene expression of many immunological molecules. In scalp LS the most significantly upregulated genes in scalp LS include S100A12, DEFB4, IL1F9 (encoding IL-36?) and IL8 (all increased >20-fold compared to scalp LS) and all genes regulated by IL-17, such as OASL, KYN4, PI3, CCL20, S100A9, LCN2, CXCL9, IFI27 and OAS1. As part of the genetic comparisons, we found that the underlying NL scalp of psoriasis had genetic expressions intermediate between the LS and N scalp, implying low levels of inflammation in this tissue. In cutaneous psoriasis, many other genes are highly represented in the cutaneous transcriptome. Differences were found in LCN2, KRT6 are all highly upregulated in LS psoriasis vulgaris, 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 tissue had lower expression of CD1A and CD207/langerin (clusters 2 and 3), which are markers of LC. The LCN2 gene encodes lipocalin-2, a protein involved in innate immunity that sequesters iron and consequently limits bacterial growth. Lipocalin-2 is expressed in neutrophils, monocytes, and keratinocytes; its serum levels are increased in patients with psoriasis and are related to the severity of the disease.KLK6 encodes a serine protease with activity against extracellular matrix proteins, such as fibronectin, laminin, vitronectin, and collagen, and is elevated in both psoriatic arthritis synovial fluids and psoriatic plaques. Therefore, genes induced by TNFα, 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 disease transcriptome genes were slightly higher in skin LS compared to scalp LS, a finding that may be explained by constitutive expression of some psoriatic transcriptome genes in the epithelium. follicle of the NLscalp. To estimate changes in pathway activity in scalp psoriasis transcriptomes, we performed GSVA. Were scalp transcriptomes particularly enriched with “basal vs upper epidermis,” “melanocytes,” “fibroblasts,” and “CD4+ T cells” and INF-activated keratinocytes profiles? or IL-13 and IL-17-induced myeloid DCs. 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 cells”, “PBMCs”, “macrophages”, “mature DCs”, “Immature DCs”', 'Th17', 'Th22' and gene sets related to TNFα/IL-17/IL-22-induced keratinocyte responses. When comparing immune gene sets using 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 human disease. In our case, the IL-23-induced murine transcriptome showed the greatest similarity to human skin and scalp psoriasis. Although the scalp is considered more similar to the skin of animal models, psoriasis remains an IFL skin disease even in the scalp. 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 LS psoriasis samples than in NL scalp psoriasis samples, as previously described for LS psoriasis . We also analyzed the mRNA of IL-20, a cytokine produced by inflammatory dendritic cells (iDCs) that influences keratinocyte activation and proliferation, and found it to be significantly higher in LS scalp samples compared to NL ones. Increased mRNA expression of iNOS, an inducible nitric oxide synthase produced by Tip-DC, was also observed in LS scalp, similar to previous reports on skin psoriasis. We also analyzed the immunophenotypic profiles of scalp and skin psoriasis compared to AA and AD. Scalp psoriasis showed a Th1/Th17 activation profile, similar to skin psoriasis, but with more Th1 and less Th22 activation. We also found significant differences compared to AA, which shows Th1/Th2 and IL-23 polarization and a lack of Th17 or Th22, and AD, which shows increased expression of Th2/Th22 cytokines. These studies have examined scalp psoriasis at the genetic level, but information at the protein level is lacking even in light of the fact that various proteins and genes are biomarkers implicated in psoriasis. The S100A8-S100A9 protein complex mediates psoriasis by regulating the expression of complement factor C3 (Schonthaler HB et al.,.