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Psoriasis Drug project

Psoriasis /sɵˈraɪ.əsɨs/ is a long lasting disease characterized by patches of abnormal skin.[1] These skin patches are typically red, itchy, and scaly. They may vary in severity from small and localized to complete body coverage.[2] Injury to the skin can trigger psoriatic skin changes at that spot, known as Koebner phenomenon.[3] Psoriasis is associated with an increased risk of psoriatic arthritis, lymphomas, cardiovascular disease, Crohn's disease and depression.[4] Psoriatic arthritis affects up to 30% of individuals with psoriasis.[5]

There are five main types of psoriasis: plaque, guttate, inverse, pustular, and erythrodermic.[1] Plaque psoriasis, also known as psoriasis vulgaris, is about 90% of cases. It typically presents with red patches with white scales on top. Most commonly affected areas are the back of the forearms, shins, around the belly button, and scalp.[4] Guttate psoriasis has drop shapped lesions.[1] Pustular psoriasis presents with small non-infectious pus filled blister.[5] Inverse psoriasis forms red patches in skin folds.[1] Erytherodermic psoriasis is when the rash becomes very widespread and can develop from any of the other types. Fingernails and toenails are affected in most people at some point in time. This may include pits in the nails or changes in color.[4]

Psoriasis is generally considered a genetic disease which is triggered by environmental factors.[2] In twin studies, identical twins are three times more likely to both be affected compared to non-identical twins; this suggests that shared genetic risk factors predispose to psoriasis. Symptoms often worse during winter and with certain medications such as beta blockers or NSAIDs.[4] Infections and psychological stress may also play a role.[2][1] Psoriasis is not contagious. The underlying mechanism involves the immune system reacting to skin cells. Diagnosis is typically based on the signs and symptoms.[4]

There is no cure for psoriasis. Various treatments; however, can help control the symptoms.[4] These treatments may include steroid creams, vitamin D3 cream, ultraviolet light, and immunosuppresent medication such as methotrexate.[1] About 75% of people can be managed with creams alone.[4] The disease affects 2–4% of the population.[6] Both males and females are affected with equal frequency.[1]


Around one-third of people with psoriasis report a family history of the disease, and researchers have identified genetic loci associated with the condition. Identical twin studies suggest a 70% chance of a twin developing psoriasis if the other twin has the disorder. The risk is around 20% for nonidentical twins. These findings suggest both a genetic susceptibility and an environmental response in developing psoriasis.[25]

Psoriasis has a strong hereditary component, and many genes are associated with it, but it is unclear how those genes work together. Most of the identified genes relate to the immune system, particularly the major histocompatibility complex (MHC) and T cells. Genetic studies are valuable due to their ability to identify molecular mechanisms and pathways for further study and potential drug targets.[26]

Classic genome-wide linkage analysis has identified nine loci on different chromosomes associated with psoriasis. They are called psoriasis susceptibility 1 through 9 (PSORS1 through PSORS9). Within those loci are genes on pathways that lead to inflammation. Certain variations (mutations) of those genes are commonly found in psoriasis.[26] Genome-wide association scans have identified other genes that are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.[26]

The major determinant is PSORS1, which probably accounts for 35%–50% of psoriasis heritability. It controls genes that affect the immune system or encode skin proteins that are overabundant with psoriasis. PSORS1 is located on chromosome 6 in the major histocompatibility complex (MHC), which controls important immune functions. Three genes in the PSORS1 locus have a strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6,[27] which encodes a MHC class I protein; CCHCR1, variant WWC, which encodes a coiled protein that is overexpressed in psoriatic epidermis; and CDSN, variant allele 5, which encodes corneodesmosin, a protein which is expressed in the granular and cornified layers of the epidermis and upregulated in psoriasis.[26]

Two major immune system genes under investigation are interleukin-12 subunit beta (IL12B) on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor, and is involved in T cell differentiation. Interleukin-23 receptor and IL12B have both been strongly linked with psoriasis.[27] T cells are involved in the inflammatory process that leads to psoriasis.[26] These genes are on the pathway that up-regulate tumor necrosis factor-α and nuclear factor κB, two genes involved in inflammation.[26] Recently, the first gene directly linked to psoriasis has been identified. A rare mutation in the gene encoding for the CARD14 protein plus an environmental trigger was enough to cause plaque psoriasis (the most common form of psoriasis).[28][29]

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