Elevated levels of endogenous apoptotic DNA and IFN-alpha in complement C4-deficient mice: implications for induction of systemic lupus erythematosus.
Eur J Immunol
; 37(6): 1702-9, 2007 Jun.
Article
en En
| MEDLINE
| ID: mdl-17506029
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-alpha seems to be a key cytokine in SLE as an activated IFN-alpha 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-alpha. 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-alpha.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Complemento C4
/
ADN
/
Interferón-alfa
/
Apoptosis
/
Lupus Eritematoso Sistémico
Idioma:
En
Revista:
Eur J Immunol
Año:
2007
Tipo del documento:
Article
País de afiliación:
Alemania