Interferon (IFN) signature genes have been shown to be expressed highly in 
peripheral blood of patients with systemic lupus erythematosus (SLE), especially 
in the presence of active disease. However, the expression of this gene 
signature in individuals with incomplete forms of lupus and the pathogenic 
relationship between IFN signature genes and autoantibody production have not 
been explored fully. In the present study, we examined the gene expression and 
autoantibody profiles of patients diagnosed with incomplete lupus erythematosus 
(ILE) to determine correlations of the gene expression signature with 
autoantibody production. Gene expression analysis was carried out on the 24K 
Illumina Human Refseq-8 arrays using blood samples from 84 subjects, including 
patients with SLE (n = 27) or ILE (n = 24), first-degree relatives (FDR) of 
these patients (n = 22) and non-autoimmune control (NC) individuals (n = 11). 
Autoantibody expression was measured using standard immunoassays and autoantigen 
proteomic arrays. Up-regulation of a set of 63 IFN signature genes was seen in 
83% of SLE patients and 50% of ILE patients. High levels of IFN gene expression 
in ILE and SLE showed significant correlations with the expression of a subset 
of IgG autoantibodies, including chromatin, dsDNA, dsRNA, U1snRNP, Ro/SSA, 
La/SSB, topoisomerase I and Scl 70, while low IFN levels were correlated with 
immunoglobulin (Ig)M autoreactivity. These studies suggest that in patients with 
ILE the IFN gene expression signature may identify a subset of these individuals 
who are at risk for disease progression. Furthermore, high levels of alpha IFN 
may promote autoantibody class-switch from IgM to the more pathogenic IgG class.