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Systemic lupus erythematosus (SLE) is a heterogeneous disorder with associated morbidity and mortality. It has long has been believed that patients are genetically predisposed to develop SLE, and evidence of this heritability is often observed in family members of LE patients. Interferon-α (IFN-α) is able to break immunologic self-tolerance by activating antigen-presenting cells after the uptake of self material. In addition, IFN-α levels are known to be elevated in SLE patients and to correlate with LE activity. Patients receiving IFN-α for malignancy or chronic hepatitis may develop de novo SLE that resolves when the drug is withdrawn.
To determine whether high serum IFN-α activity is a cause or a result of the disease, investigators compa…