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Study reveals two genes linked to disabling arthritis
2007-10-21 13:25:30 Xinhua English

WASHINGTON, Oct. 21 (Xinhua) -- An international team of researchers led by geneticists at Fred Hutchinson Cancer Research Center in Seattle has discovered two genes linked to a disabling form of arthritis called ankylosing spondylitis, a painful and progressive disease in which some or all of the spine's vertebrae fuse together.

The researchers also validated the association of two genes implicated in Graves' disease, an autoimmune condition that causesover activity of the thyroid gland. The findings were reported online in Nature Genetics on Sunday.

The study revealed two genes linked to ankylosing spondylitis: ARTS1 and IL23R, both of which influence immune function. Together with the previously known gene HLA-B27, the new findings increase to three the number of genes known to be involved in the disease.

A person who carries all three genetic variants would be expected to have a one-in-four chance of developing the disease, said the study.

The discovery of both genes, as well as the validation of two prime genetic suspects in Graves' disease -- genes known as TSHR and FCRL3 -- arose from a comprehensive scan of the human genome in which dozens of researchers used genotyping technology to analyze DNA samples from thousands of patients suffering from a variety of common diseases and compared them to DNA from a similar number of healthy control subjects.

Ankylosing spondylit is not only affects the spine but also can attack other joints and organs, including the heart, lungs and eyes. The condition afflicts an estimated one in 200 males and one in 500 females and typically strikes during adolescence and young adulthood.

Previous research also has linked IL23R with inflammatory-bowel disease (Crohn's disease) and psoriasis.

"Clinically these diseases tend to occur together -- people with inflammatory-bowel disease also tend to have a higher probability of having ankylosing spondylitis and psoriasis. The IL23R gene provides a genetic link that sheds new light on their co-occurrence," said Cardon of the Hutchinson Center.

With these new clues in hand, researchers next will study the genes in model organisms to work out the pathways by which they cause disease. The ultimate goal is improved diagnostics and drug discovery to those diseases.

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