Elevated levels of endogenous apoptotic DNA and IFN-α in complement C4-deficient mice: Implications for induction of systemic lupus erythematosus

Doreen Finke, Katharina Randers, Robert Hoerster, Holger Hennig, Rainer Zawatzky, Tony Marion, Christian Brockmann, Katja Klempt-Giessing, Kirsten Jacobsen, Holger Kirchner, Siegfried Goerg*

*Korrespondierende/r Autor/-in für diese Arbeit
11 Zitate (Scopus)

Abstract

Systemic lupus erythematosus (SLE), an autoimmune disease characterized by chronic nephritis, arthritis and dermatitis, and the presence of antinuclear autoantibodies, is associated with complement factor deficiencies in the classical activation pathway. In addition, IFN-α seems to be a key cytokine in SLE as an activated IFN-α system is regularly observed in patients with SLE. Here, we demonstrate that in lupus-susceptible, complement C4-deficient mice the lack of complement results in elevated intravascular levels of apoptotic DNA. The apoptotic DNA is targeted to the splenic marginal zone where it accumulates and induces IFN-α. As such, we present here a unifying hypothesis for the induction of SLE that incorporates the role of complement deficiency and elevated levels of IFN-α.

OriginalspracheEnglisch
ZeitschriftEuropean Journal of Immunology
Jahrgang37
Ausgabenummer6
Seiten (von - bis)1702-1709
Seitenumfang8
ISSN0014-2980
DOIs
PublikationsstatusVeröffentlicht - 01.06.2007

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