Systemic IFN-α drives kidney nephritis in B6.Sle123 mice

被引：77

作者：

Fairhurst, Anna-Marie ^{[1
]}

Mathian, Alexis ^{[3
]}

Connolly, John E. ^{[4
]}

Wang, Andrew ^{[1
]}

Gray, Hillery F. ^{[1
]}

George, Tiffany A. ^{[1
]}

Boudreaux, Christopher D. ^{[1
]}

Zhou, Xin J. ^{[2
]}

Li, Quan-Zhen ^{[5
]}

Koutouzov, Sophie ^{[5
]}

Banchereau, Jacques ^{[4
]}

Wakeland, Edward K. ^{[1
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Dept Immunol, Dallas, TX 75390 USA

[2] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA

[3] Hop La Pitie Salpetriere, Med Interna Serv 2, Paris, France

[4] Baylor Inst Immunol Res, Dallas, TX USA

[5] Inst Natl Sante & Rech Med, U764, Clamart, France

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2008年 / 38卷 / 07期

关键词：

Congenic; IFN; systemic lupus erythematosus;

D O I：

10.1002/eji.200837925

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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-a 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-a 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-a 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-a in this murine model is an exacerbation of mechanisms mediating end organ damage.

引用

页码：1948 / 1960

页数：13

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