Paris - Scientists have identified genes linked to psoriasis and lupus, diseases triggered by immune responses that cause painful inflammation, separate studies released on Sunday showed.
Psoriasis affects between one and four percent of the population worldwide, with sharp variations depending on geographic region.
Symptoms include red scaly patches on the skin, called psoriatic plaques, and in about 15 percent of cases swelling of the joints.
Knowing that a gene called beta-defensin can trigger skin inflammation in response to infections, a team led by John Armour, a researcher at the University of Nottingham in Britain, decided to find out if people with extra copies of the gene might be more prone to developing psoriasis.
The hunch proved to be right on target. In two separate groups examined, one in the Netherlands and the other in Germany, psoriasis sufferers had significantly more copies of the suspect gene than individuals not troubled by the skin disease.
Many diseases originate from both genetic and environmental factors, and even when genes do play a dominant role, there can be more than one culprit, making it very difficult to determine the root cause.
But linking a particular genetic variation to an illness is a key step, and can give researchers leads for new treatments, and possibly even a cure.
Lupus is a far less common disease that makes the body's immune system turn against itself, causing swelling and pain of the skin, joints and various internal organs.
Symptoms are generally mild, but in extreme cases can be life-threatening. More than 90 percent of people with lupus are women, especially during child-bearing years, between the ages of 15 and 45.
Like psoriasis, the exact cause of lupus is unknown.
A team of researchers in Britain and the United States led by Timothy Vyse of Imperial College in London showed that individuals with a particular genetic variation near a gene called TNFSF4 were at higher risk of developing lupus.
Along with the study on psoriasis, his findings were published online in the British journal Nature Genetics.
In a group of nearly 500 affected families in Britain, along with a smaller sampling in the United States, the researchers found that this set of genetic variants seemed to boost the expression of TNFSF4 in blood lymphocytes in lupus sufferers.
Lymphcytes are white blood cells which, triggered by the immune system, attack foreign objects - such as bacteria - in the body.