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Disruption of Type I-IFN Signaling Decreases Autoimmune Development and Kidney Damage, But Not Anxiety-Like Behaviors in Lupus NZB Mice

Hua Zhang and Jianping Wang

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder that is accompanied by neuropsychiatric manifestations such as anxiety. Despite undefined etio-pathogenesis for SLE, emerging evidence supports the importance of type I interferon (IFN) in the pathogenesis of autoimmune formation and renal damage both in SLE patients and lupus mice. Linkage mapping identified a quantitative trait locus (QTL) for elevated plus-maze (EPM) performance on the segment of chromosome 4 in lupus-prone New Zealand black (NZB) mice where the type I IFN-α genes are harbored. To determine possible roles of type I IFNs for anxiety-like behaviors in NZB mice, we evaluated the anxiety profile by EPM test in NZB mice with deficiency of type I-IFN receptor (IFNARKO). Consistent with previous observation, disruption of the type I-IFN signaling resulted in a dramatic attenuation in glomerulonephritis, splenomegaly and plasma anti-nuclear antibodies (ANA) in NZB mice. However, blockade of type I-IFN signaling had no effect on performance in the EPM by NZB/IFNARKO mice in comparison to wild type controls. The results support a pathogenic role for type I-IFN in autoimmune development and kidney inflammation. Nonetheless, type I-IFN signaling is not responsible for increased anxiety profile developed in these autoimmune mice.