| First Author | Lee PY | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 7 | Pages | 5101-8 |
| PubMed ID | 18354236 | Mgi Jnum | J:133377 |
| Mgi Id | MGI:3778346 | Doi | 10.4049/jimmunol.180.7.5101 |
| Citation | Lee PY, et al. (2008) A Novel Type I IFN-Producing Cell Subset in Murine Lupus. J Immunol 180(7):5101-8 |
| abstractText | 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 Ly6C(high) 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 Ly6C(high) 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. |
