Possible ‘master switch’ gene found in juvenile arthritisJuly 2nd, 2008 - 5:20 pm ICT by ANI
Washington, July 2 (ANI): Researchers at The Children’s Hospital of Philadelphia have found that a gene region known to play a role in some varieties of adult rheumatoid arthritis is also present in all types of childhood arthritis.
They said that the responsible gene may be a master switch that helps turn on the debilitating disease.
The genetic variant is on chromosome 9 in a region housing two genes, TRAF1 and C5.
The TRAF1 gene codes for a protein that regulates tumour necrosis factor, a chemical strongly associated with juvenile idiopathic arthritis (JIA), formerly called juvenile rheumatoid arthritis.
However, the researchers said that further study is required to determine whether the TRAF1 gene or the C5 gene is altered in the disease.
“There are only a few genes that may act as master switches like this to regulate autoimmune diseases,” said lead author Terri H. Finkel, the chief of Rheumatology at Children’s Hospital.
“This switch we discovered probably has to be an ‘ON’ gene and when it interacts with other genes and environmental triggers, a child may get juvenile arthritis,” Finkel added.
For the study, researchers compared 67 Caucasian patients being treated for JIA to 1,952 healthy Caucasian control subjects recruited within the hospital’s patient network.
While the cause of JIA is unknown, results from this study back up past research that shows arthritis arises in a genetically susceptible individual due to environmental factors.
Edward M. Behrens, a paediatric rheumatologist at Children’s Hospital, said: “We think this finding may be a clue to the specific disease pathway that leads to arthritis,
“We currently use medicines called tumour necrosis factor blockers to treat children with JIA. However, not all children respond to these drugs, and other children may develop severe allergic reactions and other side effects. If we can fully identify all the genes that interact with environmental risk factors, we might develop more targeted treatments with fewer side effects,” he added.
Co-author Hakon Hakonarson said: “The high-resolution genome-wide association approach has very markedly enhanced our ability to identify disease genes in complex disorders such as JIA, and what is remarkable about this discovery is that it appears there may be a common genetic factor predisposing to all seven forms of the disease.
The study appears in the July 2008 issue of Arthritis & Rheumatism. (ANI)
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