The research, which has just been published in the journal Nature Genetics, shows that people who lack the genes LCE3B and LCE3C are more likely to be affected by psoriasis.
These two genes appear to be involved in the skin’s response to damage. When these genes are missing this may leave skin relatively unprotected against the sequence of damage and inflammation that leads to the development of this uncomfortable skin disease.
John Armour, Professor of Human Genetics in the Institute of Genetics, together with Master of Research student Emma Dannhauser, were involved because of their expertise in accurate measurement of gene numbers.
Professor Armour said: "Measuring gene numbers accurately is technically challenging but is necessary to demonstrate this kind of effect. This new report adds to the growing number of examples of disorders caused by variation in the number of genes, and suggests that there may be many more examples to come. What's especially interesting about this example is that in the UK lacking these genes is actually commoner than having them."
Around 30 per cent of people with psoriasis have a family history of the condition. It has long been known that genetic predisposition is an important cause of psoriasis, but it is only recently that scientists have begun to discover the exact nature of the variations that give rise to that predisposition.
The study is the result of an international collaboration led by Professor Xavier Estivill at Pompeu Fabra University in Barcelona, and involving scientists from Nottingham, Nijmegen, St Louis, San Francisco, Michigan, Seattle, Rome and Evry in France.
Psoriasis is a common skin condition affecting about two per cent of the UK population, and causes patches of scaly, itchy skin. It generally affects prominent areas such as the elbows and knees, and commonly affects the scalp, but can affect any part of the skin.
Last year Professor Armour headed a research project, also published in Nature Genetics, which showed that psoriasis risk was affected by variation in the number of beta-defensin genes — a gene known to trigger skin inflammation in response to infection. The research established that people with extra copies of the gene might be more prone to developing psoriasis.
Emma Thorne | alfa
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