Review for "Dnase1 -deficient mice spontaneously develop a Systemic Lupus Erythematosus-like disease"

Author(s):  
Elaine F. Kenny ◽  
Bärbel Raupach ◽  
Ulrike Abu Abed ◽  
Volker Brinkmann ◽  
Arturo Zychlinsky

2007 ◽  
Vol 37 (6) ◽  
pp. 1702-1709 ◽  
Author(s):  
Doreen Finke ◽  
Katharina Randers ◽  
Robert Hoerster ◽  
Holger Hennig ◽  
Rainer Zawatzky ◽  
...  

2010 ◽  
Vol 34 (4) ◽  
pp. 339-348 ◽  
Author(s):  
Marie-Laure Santiago-Raber ◽  
Isabelle Dunand-Sauthier ◽  
Tianfu Wu ◽  
Quan-Zhen Li ◽  
Satoshi Uematsu ◽  
...  

1998 ◽  
Vol 188 (7) ◽  
pp. 1247-1254 ◽  
Author(s):  
Hui Xu ◽  
Hui Li ◽  
Elisabeth Suri-Payer ◽  
Richard R. Hardy ◽  
Martin Weigert

Anti-DNA antibodies are regulated in normal individuals but are found in high concentration in the serum of systemic lupus erythematosus (SLE) patients and the MRL lpr/lpr mouse model of SLE. We previously studied the regulation of anti–double-stranded (ds)DNA and anti–single-stranded (ss)DNA B cells in a nonautoimmune background by generating mice carrying immunoglobulin transgenes coding for anti-DNAs derived from MRL lpr/lpr. Anti-dsDNA B cells undergo receptor editing, but anti-ssDNA B cells seem to be functionally silenced. Here we have investigated how anti-DNA B cells are regulated in recombination- activating gene (RAG)-2−/− mice. In this setting, anti-dsDNA B cells are eliminated by apoptosis in the bone marrow and anti-ssDNA B cells are partially activated.


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