| Literature DB >> 18506882 |
Anna-Marie Fairhurst1, Alexis Mathian, John E Connolly, Andrew Wang, Hillery F Gray, Tiffany A George, Christopher D Boudreaux, Xin J Zhou, Quan-Zhen Li, Sophie Koutouzov, Jacques Banchereau, Edward K Wakeland.
Abstract
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.Entities:
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Year: 2008 PMID： 18506882 PMCID： PMC2699327 DOI： 10.1002/eji.200837925
Source DB: PubMed Journal: Eur J Immunol ISSN： 0014-2980 Impact factor: 5.532