Heterophile Antibodies Masquerade as Interferon-α in Subjects With New-Onset Type 1 Diabetes
- Theresa Aly, MD,
- Devasenan Devendra, MRCP,
- Jennifer Barker, MD,
- Edwin Liu, MD,
- Liping Yu, MD and
- George S. Eisenbarth, MD, PHD
- From the Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, Colorado.
- Address correspondence and reprint requests to Dr. D. Devendra, Postdoctoral fellow, Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, 4200 East 9th Ave., Box B-140, Denver, CO 80262. E-mail: devasenan.devendra{at}uchsc.edu
One of the potential environmental triggers in type 1 diabetes may be viruses. The mechanism of viral infections leading to β-cell destruction of the pancreas is becoming clearer, and the potential role of viruses inducing the cytokine interferon-α (IFN-α) has been implicated. It is well established that IFN-α therapy induces islet cell autoimmunity and other endocrine autoantibodies as well (1). Recent studies have indicated that IFN-α levels in serum of new-onset type 1 diabetic subjects are elevated and perhaps related to recent enteroviral infections (2,3). These studies suggest that IFN-α may be a useful surrogate marker for disease onset, perhaps due to a recent viral infection or vaccination.
At the Barbara Davis Center for Childhood Diabetes in Denver, Colorado, we screened 32 new-onset type 1 diabetic subjects and 31 …
