Several lines of evidence link the Interferons to systemic autoimmune diseases, including Systemic Sclerosis (SSc), Sjogren syndrome (SjS), and Systemic Lupus Erythematosus (SLE) through activation of the so-called "interferon signature". Among the interferon-inducible genes, a gene family encodes evolutionarily related human proteins designated IFI16, IFIX, MNDA, and AIM2. We have previously demonstrated that oxidative stress and various proinflammatory cytokines can trigger IFI16 expression. In addition, a role of IFI16 as an inducer of proinflammatory molecules in endothelial cells has also been observed, supporting its role in the initial steps of the inflammatory process that precedes the onset of autoimmune syndromes. IFI16 protein is also a target for autoantibodies. In this study, we report the results obtained by looking at the levels of anti-IFI16 antibodies (in house ELISA) in patients with autoimmune diseases, including SSc, SjS and SLE. Anti-IFI16 antibodies were detected in SLE (56%), SjS (50%) and in 30% of the SSc patients who tested negative for both ACAs and anti-topo I antibodies. In this subgroup of patients, they were significantly associated with the limited cutaneous form of SSc with a sensitivity of 40% and a specificity of 81%. Moreover, analysis of the distribution of anti-RNAP III antibodies vs anti-IFI16 in the same SSc population showed that they were mutually exclusive. Overall, our findings indicate that anti-IFI16 autoantibodies are frequently detected in autoimmune diseases, displaying clinical and laboratory correlations, and being particularly useful for diagnosis and disease classification in patients who are negative for other SSc serological markers.
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