An international research team has published data from a group of studies, which have uncovered new genetic variants associated with the autoimmune disease, psoriasis.
Psoriasis affects approximately two to three percent of the European population and is caused when the body's immune system signals the skin cells to divide at a higher rate than normal. The most common form of the disease, psoriasis vulgaris, causes scaly, itchy patches of skin to form, which are often uncomfortable and can be painful.
One of the published studies, conducted by scientists from the Genetic Analysis of Psoriasis Consortium and the Wellcome Trust Case Control Consortium Two performed a genome-wide association study (GWAS) on individuals with psoriasis and a control group free from the condition, looking for small genetic variations known as SNPs (single nucleotide polymorphisms).
They uncovered eight regions not previously identified with psoriasis, including seven regions known to contain genes linked with immune function. Six of these were confirmed by an earlier European study that analysed the genomes of over 9,000 people.
The scientists also discovered evidence of a strong interaction between two independent genetic regions, HLA-C and ERAP1 associated with the condition, which - when linked in this way - are thought to greatly increase the risk of developing the disease.
Professor Richard Trembath from King’s College, London who co-led the study said: 'Through our research, and other studies now coming through, the research community have identified genes that play a role in people's susceptibility to the condition'.
At present, treatment options for psoriasis are limited and complex, but experts hope that this new information may provide new leads for the development of better treatment for psoriasis and related disorders.
Dr James Elder of the University of Michigan Health System who leads a related American study said: 'The goal is to guide the pharmaceutical companies toward a better understanding about which cells are working and which ones are causing trouble so that medicines can be made to stop the trouble'.
The results were reported across five papers published in the journal Nature Genetics.
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