title: Type I interferon correlates with serological and clinical manifestations of SLE.
abstract: BACKGROUND
  Systemic lupus erythematosus (SLE) is an autoimmune disease affecting multiple organ systems triggered by the production of autoantibodies. Previous clinical studies in humans and murine models suggest that type I interferons (IFNs) are important for the initiation and potentiation of SLE activity.
  
  
  METHODS
  65 consecutive patients with SLE were identified from the University of California, San Francisco Lupus Clinic with moderate-severe disease activity. 94 serological samples were collected. Type I IFN levels and the ability of plasma to induce expression of several surface markers of dendritic cell maturation were measured.
  
  
  RESULTS
  Type I IFN levels correlated with the presence of cutaneous manifestations, and there was a trend towards correlation with renal disease. No correlation was found between type I IFN levels and neurological disease. Type I IFN levels correlated positively with the SLEDAI score and anti-dsDNA levels and inversely with C3 levels. Interestingly, type I IFN levels were highest in African American patients. SLE plasma also induced the expression of MHC class I, CD38, and CD123 on monocytes, and was blocked by the addition of a monoclonal antibody to IFNAR1.
  
  
  CONCLUSIONS
  The pathogenic role of type I IFN is suggested by the induction of cell surface markers for dendritic cell maturation. The potential therapeutic utility of antibodies directed to either type I IFN or IFNAR1/IFNAR2 may be of interest in further studies.
authors.affiliation: University of California, San Francisco, San Francisco, CA 94143, USA.
authors.forename: M C
authors.initials: MC
authors.lastname: Dall'era
authors.forename: P M
authors.initials: PM
authors.lastname: Cardarelli
authors.forename: B T
authors.initials: BT
authors.lastname: Preston
authors.forename: A
authors.initials: A
authors.lastname: Witte
authors.forename: J C
authors.initials: JC
authors.lastname: Davis
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D000974:Antibodies, Antinuclear / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002454:Cell Differentiation; D003176:Complement C3 / Q000032:analysis; D003713:Dendritic Cells / Q000473:pathology; D005260:Female; D006801:Humans; D007370:Interferon Type I / Q000097:blood*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology; D008180:Lupus Erythematosus, Systemic / Q000208:ethnology / Q000276:immunology*; D008181:Lupus Nephritis / Q000276:immunology; D020945:Lupus Vasculitis, Central Nervous System / Q000276:immunology; D008297:Male; D008565:Membrane Proteins / Q000276:immunology; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000473:pathology; D053633:Receptor, Interferon alpha-beta; D017471:Receptors, Interferon / Q000276:immunology; D011994:Recombinant Proteins; D012720:Severity of Illness Index
chemical_list: D000974:Antibodies, Antinuclear; D015415:Biomarkers; D003176:Complement C3; C507964:IFNAR1 protein, human; C508033:IFNAR2 protein, human; D007370:Interferon Type I; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D008565:Membrane Proteins; D017471:Receptors, Interferon; D011994:Recombinant Proteins; D053633:Receptor, Interferon alpha-beta