title: Anti-IFI16 antibodies and their relation to disease characteristics in systemic lupus erythematosus.
abstract: OBJECTIVE
  Several studies have shown the presence of anti-IFI16 antibodies in systemic lupus erythematosus (SLE), Sjögren Syndrome (SjS), systemic sclerosis (SSc) and other autoimmune diseases. However, the significance of anti-IFI16 antibodies in SLE has not been fully characterized. The aim of this study was to investigate associations between anti-IFI16 antibodies and clinical and serologic parameters of SLE.
  
  
  METHODS
  An enzyme-linked immunosorbent assay (ELISA) kit was used to measure anti-IFI16 antibodies in the sera of 168 SLE patients, 46 patients with any type of primary glomerulonephritis (GN) and 182 healthy controls (HCs). Associations between anti-IFI16 antibodies and clinical and serologic parameters of SLE were statistically evaluated using both univariate and multivariate analysis.
  
  
  RESULTS
  Significantly higher anti-IFI16 titres were observed in SLE patients compared to both non-SLE GN and HCs (median levels: 270.1 U/ml vs 132.1 U/ml, p = 0.001, and 52.9 U/ml, p < 0.0001, respectively). With cut-off levels corresponding to the 95th percentile of the control population (113 U/ml), 63% of the SLE patients tested positive for anti-IFI16 autoantibodies, compared to just 24% of patients with primary non-SLE GN and 5% of HCs. The presence of anti-IFI16 antibodies inversely correlated with proteinuria (univariate analysis) and C3 hypocomplementaemia (univariate and multivariate analyses).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Translational Medicine, Medical School of Novara, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Caneparo
authors.forename: T
authors.initials: T
authors.lastname: Cena
authors.forename: M
authors.initials: M
authors.lastname: De Andrea
authors.forename: V
authors.initials: V
authors.lastname: Dell'oste
authors.forename: P
authors.initials: P
authors.lastname: Stratta
authors.forename: M
authors.initials: M
authors.lastname: Quaglia
authors.forename: A
authors.initials: A
authors.lastname: Tincani
authors.forename: L
authors.initials: L
authors.lastname: Andreoli
authors.forename: S
authors.initials: S
authors.lastname: Ceffa
authors.forename: M
authors.initials: M
authors.lastname: Taraborelli
authors.forename: C
authors.initials: C
authors.lastname: Magnani
authors.forename: S
authors.initials: S
authors.lastname: Landolfo
authors.forename: M
authors.initials: M
authors.lastname: Gariglio
mesh_terms: D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000276:immunology*; D016022:Case-Control Studies; D003176:Complement C3 / Q000172:deficiency; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009687:Nuclear Proteins / Q000276:immunology*; D010750:Phosphoproteins / Q000276:immunology*; D011507:Proteinuria / Q000209:etiology / Q000276:immunology
chemical_list: D000974:Antibodies, Antinuclear; D003176:Complement C3; D009687:Nuclear Proteins; D010750:Phosphoproteins; C076700:IFI16 protein, human
keywords: IFI16; Systemic lupus erythematosus; autoantibodies; interferons; proteinuria