A Novel Type I IFN-Producing Cell Subset in Murine Lupus1 (original) (raw)
Journal Article
Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
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Gainesville, FL 32610-0221
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Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
,
Gainesville, FL 32610-0221
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Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
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Gainesville, FL 32610-0221
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Department of Surgery, University of Florida
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Gainesville, FL 32610-0221
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Yi Li ,
Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
,
Gainesville, FL 32610-0221
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Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
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Gainesville, FL 32610-0221
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Department of Molecular Cell Biology, Free University Medical Center
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Amsterdam
,
The Netherlands
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Department of Surgery, University of Florida
,
Gainesville, FL 32610-0221
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Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
,
Gainesville, FL 32610-0221
Department of Pathology, Immunology and Laboratory Medicine, University of Florida
,
Gainesville, FL 32610-0221
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Division of Rheumatology & Clinical Immunology and Center for Autoimmune Disease, University of Florida
,
Gainesville, FL 32610-0221
Department of Pathology, Immunology and Laboratory Medicine, University of Florida
,
Gainesville, FL 32610-0221
Address correspondence and reprint requests to Dr. Westley H. Reeves, Division of Rheumatology & Clinical Immunology, University of Florida, PO Box 100221, Gainesville, FL 32610-0221. E-mail address: [email protected]
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Received:
11 January 2008
Accepted:
30 January 2008
Cite
Pui Y Lee, Jason S Weinstein, Dina C Nacionales, Philip O Scumpia, Yi Li, Edward Butfiloski, Nico van Rooijen, Lyle Moldawer, Minoru Satoh, Westley H Reeves, A Novel Type I IFN-Producing Cell Subset in Murine Lupus, The Journal of Immunology, Volume 180, Issue 7, April 2008, Pages 5101–5108, https://doi.org/10.4049/jimmunol.180.7.5101
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Abstract
Excess type I IFNs (IFN-I) have been linked to the pathogenesis of systemic lupus erythematosus (SLE). Therapeutic use of IFN-I can trigger the onset of SLE and most lupus patients display up-regulation of a group of IFN-stimulated genes (ISGs). Although this “IFN signature” has been linked with disease activity, kidney involvement, and autoantibody production, the source of IFN-I production in SLE remains unclear. 2,6,10,14-Tetramethylpentadecane-induced lupus is at present the only model of SLE associated with excess IFN-I production and ISG expression. In this study, we demonstrate that tetramethylpentadecane treatment induces an accumulation of immature Ly6Chigh monocytes, which are a major source of IFN-I in this lupus model. Importantly, they were distinct from IFN-producing dendritic cells (DCs). The expression of IFN-I and ISGs was rapidly abolished by monocyte depletion whereas systemic ablation of DCs had little effect. In addition, there was a striking correlation between the numbers of Ly6Chigh monocytes and the production of lupus autoantibodies. Therefore, immature monocytes rather than DCs appear to be the primary source of IFN-I in this model of IFN-I-dependent lupus.
Copyright © 2008 by The American Association of Immunologists
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