Type I interferon correlates with serological and clinical manifestations of SLE. Issue 12 (20th April 2005)

• Record Type: Journal Article
• Authors: Dall'Era, M C; Cardarelli, P M; Preston, B T; Witte, A; Davis, J C
• Is Part Of: Annals of the rheumatic diseases. Volume 64:Issue 12(2005)
• Page Start: 1692
• Page End: 1697
• Publication Date: 2005-04-20
• Subjects: CI, confidence interval -- DCs, dendritic cells -- ESR, erythrocyte sedimentation rate -- GM-CSF, granulocyte monocyte-colony stimulating factor -- IFN, interferon -- IFNAR1, α chain of the receptor for type I IFN -- ISRE-Luc, IFN stimulated response element luciferase -- MHC, major histocompatibility complex -- PBMCs, peripheral blood mononuclear cells -- PBS, phosphate buffered saline -- SLE, systemic lupus erythematosus -- SLEDAI, Systemic Lupus Erythematosus Disease Activity Index; SLEDAI -- interferon -- renal disease -- systemic lupus erythematosus; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.2004.033753
• Languages: English
• ISSNs: 0003-4967

Abstract

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.