| First Author | Faber-Elmann A | Year | 2002 |
| Journal | Clin Immunol | Volume | 105 |
| Issue | 2 | Pages | 223-32 |
| PubMed ID | 12482397 | Mgi Jnum | J:81136 |
| Mgi Id | MGI:2448114 | Doi | 10.1006/clim.2002.5279 |
| Citation | Faber-Elmann A, et al. (2002) A peptide based on an anti-DNA autoantibody downregulates matrix metalloproteinases in murine models of lupus. Clin Immunol 105(2):223-32 |
| abstractText | Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the increased production of autoantibodies and by T cell dysfunction associated with general clinical manifestations. A model of induced experimental SLE by the immunization with the human monoclonal anti-DNA 16/6Id(+) autoantibody and a model of the SLE-prone mice (NZB x NZW)F1 were used in the present study. Two peptides based on the complementarity determining regions (CDR) 1 and 3 of a murine monoclonal anti-DNA 16/6Id(+) autoantibody were shown to ameliorate spontaneous and induced SLE in mice. We demonstrate here that levels of matrix metalloproteinase (MMP)-3 and MMP-9 were elevated in plasma and kidneys of SLE-afflicted mice. Levels of both MMP-3 and MMP-9 were elevated in kidneys of mice with the 16/6Id induced experimental SLE already in the early phases of disease development. However, increased levels of only MMP-3 were detected in the plasma at the early stages of disease, while MMP-9 activity was elevated later, when clinical manifestations were already observed. Treatment of SLE-afflicted mice, with the CDR1-based peptide that ameliorates disease manifestations in mice, led to a reduction in MMP-9 activity and in MMP-3 protein levels both in plasma and in kidneys. We thus suggest that these enzymes may play a pathogenic role in the disease and may serve as markers for the determination of disease progression or amelioration. |
