Anti-IFI16 antibodies and their relation to disease characteristics in systemic lupus erythematosus

Abstract

The inverse correlations observed between anti-IFI16 positivity, proteinuria and C3 hypocomplementaemia suggest that anti-IFI16 antibodies do not contribute to renal inflammation in SLE; indeed they may even prevent complement consumption. Anti-IFI16 antibodies hold the potential to serve as a new biomarker of disease activity in SLE.

Mislocalization of the interferon inducible protein IFI16 by environmental insults: Implications in autoimmunity

“…Overexpression of the IFI16 autoantigen in the epidermis and inflammatory dermal infiltrates is quite evident in skin biopsies from SLE and SSc patients, while the expression levels of anti-IFI16 autoantibodies can also be found and being exploited to diagnose and differentiate between limited and diffuse cutaneous SSc [16,22]. In a statistical study, 29% SSc and 63% SLE population tested positive for significantly higher anti-IFI16 autoantibodies, while this data could be correlated to disease characteristics [22,23]. The exact involvement of IFI16 in the development of autoimmunity remains obscure, but several data implicate its role in onset of inflammation when overexpressed in endothelial cells including its role in apoptosis through the NF-kB mediated activation of caspase2 and caspase3 [24].…”

The emerging role of human PYHIN proteins in innate immunity: Implications for health and disease

“…IFI16 is a target for autoantibodies and several studies have shown the presence of anti-IFI16 autoantibodies in chronic autoimmune diseases such as SLE [64], systemic sclerosis [65], rheumatoid arthritis [66] and Sjö gren's syndrome [67]. IFI16 is known to relocalise from the nucleus to the cytosol following UV treatment or viral DNA detection.…”

Relevance of Interferon‐Inducible Protein‐16 Rather than Anti–Interferon‐Inducible Protein‐16 Autoantibodies as a Clinical and Pathogenic Biomarker in Primary Sjögren's Syndrome: Comment on the Article by Baer et al

“…In this setting, the arbitrarily high cutoff of ANA positivity chosen by Baer and colleagues (1:320, and not the usually employed approximately one-third of primary SS patients display circulating anti-IFI16 autoantibodies, the pathogenic and clinical meaning of which remains, however, rather obscure. Some studies, in fact, suggested a protective rather than proinflammatory role of anti-IFI16 autoantibodies (8,9). On the contrary, there is consistent evidence for a pathogenic role of IFI16 protein in triggering and perpetuating inflammation in some chronic inflammatory and autoimmune rheumatic disorders (10).…”