into the clinical significance of the observed autoantibody clusters. The Ro/La cluster observed here in SLE patients is similar to that of Sjogren’s Syndrome, in which 75% of the patients also show PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/22189597 autoantibodies against Ro52, Ro60 and La. Since 5/6 autoantigens 
used for clustering represent known RNA binding proteins, further understanding the details of these RNA-binding proteins and pathways may lead to additional insights into the mechanisms and/or triggers involved in both SLE and SjS. Based on the available patient information, two interesting clinical correlations emerged from our analysis of LIPS serological profiles outside the autoantibody clusters. First, within the cohort at large, anti-RNP-70k autoantibodies were significantly associated with musculoskeletal manifestations, and anti-RNP-70k, RNP-A and Sm autoantibodies with mucocutaneous symptoms. To our knowledge, the association of these autoantibodies with mucocutaneous symptoms has not yet been reported, but anti-RNP autoantibodies have previously been associated with musculoskeletal symptoms in African-American patients and with Raynaud’s phenomenon in Chinese patients. While an association between the Ro/La patient cluster and an increased prevalence of sicca symptoms was observed by To and Petri, the prevalence of sicca symptoms was not available for this cohort. Since primary SjS patients also have high titer autoantibodies to Ro52, Ro60 and La, future large scale genetic studies may provide additional clues to the similarities and differences between SjS and SLE patients within the Ro/La autoantibody cluster. The lack of clinical correlates with our autoantibody SLE data also suggests that these major diagnostic SLE antigens are likely not to be informative for identifying patients with pulmonary, renal, CNS, and hematologic symptoms. It is likely that the inclusion of other organ-specific antigens would be needed to identify clinically relevant subtypes. For example, aactinin, might be incorporated in LIPS testing to identify patients with lupus nephritis. Future studies expanding the antigen panels in the LIPS format to more comprehensively target specific organ systems may yield additional insight into the full range of lupus symptomatology. Elevated levels of interferon proteins and/or activity are associated with up-regulation of interferon-inducible genes and are thought to contribute to the pathophysiology of SLE. Seropositive anti-IFN-v autoantibodies were detected in 29% and 38% of the SLE patients in the pilot and second cohort, respectively. These autoantibodies have been observed in previous studies of SLE but at much lower frequencies, most likely due to limitations of the get Ancitabine (hydrochloride) detection methods employed. AntiIFN-v autoantibodies have been reported in several other autoimmune diseases, including in late-onset myasthenia gravis, and are associated with mutations in the autoimmune regulator gene in autoimmune polyendocrine syndrome type 1. Together, these observations suggest that anti-IFN-v autoantibodies may play a role in immune mediated disease. Anti-IFN-v positive patients also had significantly higher titers of anti-Sm, RNP-A and RNP-70k autoantibodies and were more frequently positive for anti-dsDNA in comparison to those patients without anti-IFN-v autoantibodies, suggesting an overall increased autoantibody burden in this group. In our study, a significantly higher prevalence of anti-IFN-a autoantibodies was detected in the SACQ group in comparison