| First Author | Fairhurst AM | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 7 | Pages | 1948-60 |
| PubMed ID | 18506882 | Mgi Jnum | J:137291 |
| Mgi Id | MGI:3798727 | Doi | 10.1002/eji.200837925 |
| Citation | Fairhurst AM, et al. (2008) Systemic IFN-alpha drives kidney nephritis in B6.Sle123 mice. Eur J Immunol 38(7):1948-60 |
| abstractText | The impact of IFN-alpha secretion on disease progression was assessed by comparing phenotypic changes in the lupus-prone B6.Sle1Sle2Sle3 (B6.Sle123) strain and the parental C57BL/6 (B6) congenic partner using an adenovirus (ADV) expression vector containing a recombinant IFN-alpha gene cassette (IFN-ADV). A comprehensive comparison of cell lineage composition and activation in young B6 and B6.Sle123 mice revealed a variety of cellular alterations in the presence and absence of systemic IFN-alpha. Most IFN-alpha-induced phenotypes were similar in B6 and B6.Sle123 mice; however, B6.Sle123 mice uniquely exhibited increased B1 and plasma cells after IFN-alpha exposure, although both strains had an overall loss of mature B cells in the bone marrow, spleen and periphery. Although most of the cellular effects of IFN-alpha were identical in both strains, severe glomerulonephritis occurred only in B6.Sle123 mice. Mice injected with IFN-ADV showed an increase in immune complex deposition in the kidney, together with an unexpected decrease in serum anti-nuclear antibody levels. In summary, the predominant impact of systemic IFN-alpha in this murine model is an exacerbation of mechanisms mediating end organ damage. |
