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NEW YORK (Reuters Health) Aug 21 - High serum interferon-alpha activity is apparently a heritable risk factor for systemic lupus erythematosus (SLE), according to a recent study. This finding may eventually help predict risk for SLE, researchers report.
Dr. Timothy B. Niewold from the Mary Kirkland Center for Lupus Research, Hospital for Special Surgery, New York, and colleagues analyzed IFN-alpha levels in stored serum samples from 266 patients with SLE, 359 healthy first-degree relatives, and 106 healthy unrelated controls.
The team found that 47% of SLE patients had high serum interferon-alpha activity, which is similar to previous reports. Moreover, 18% of healthy first-degree relatives also had high IFN-alpha levels, compared with just 4.5% of unrelated controls.
"High interferon-alpha activity was clustered in specific families in both SLE patients and their healthy first-degree relatives, suggesting a heritable trait," the investigators write in the September issue of Genes and Immunity. "Heritability was also supported by quantitative familial correlation of interferon-alpha activity, concordance in affected sib pairs and frequent transmission of the high IFN-alpha activity trait from parents to offspring."
They also note that the frequency of high interferon-alpha activity was similar across all ethnic backgrounds studied, including Asian or Pacific Rim, African-American, European American, Hispanic, and Native American.
Autoantibodies to RNA-binding protein and double-stranded DNA, which are relatively specific for SLE and other autoimmune diseases such as Sjogren's syndrome, correlated strongly with increased interferon-alpha activity in SLE patients. These autoantibodies were rarely seen in healthy family members and did not explain the observed familial correlations.
In a statement, Dr. Niewold, who is now with the University of Chicago, noted that the finding that many healthy family members have high levels of interferon-alpha suggests that high interferon-alpha activity doesn't always cause SLE.
"We think, however, that those levels somehow prime the immune system, lowering the threshold, so that when the wrong stimulus comes along, the cells of the immune system begin making the autoantibodies and the person develops SLE," he said.
Study co-author Dr. Mary K. Crow added, "The hope is that we may be able to use interferon-alpha levels as a measurement to predict who might be at risk to develop this disease. We can't do that yet, but the success of this study is very encouraging."
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