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Logo of arthrestherBioMed Centralbiomed central web sitesearchsubmit a manuscriptregisterthis articleArthritis Research & Therapy
 
Arthritis Res Ther. 2003; 5(2): R114–R121.
Published online Feb 3, 2003.
PMCID: PMC165037
The VH gene repertoire of splenic B cells and somatic hypermutation in systemic lupus erythematosus
Nicola LW Fraser,corresponding author1 Gary Rowley,1 Max Field,2 and David I Stott1
1Division of Immunology, Infection and Inflammation, University of Glasgow, Western Infirmary, Glasgow, Scotland, UK
2Department of Rheumatic Diseases, Glasgow Royal Infirmary, Glasgow, Scotland, UK
corresponding authorCorresponding author.
Nicola LW Fraser: nw21y/at/clinmed.gla.ac.uk
Received September 27, 2002; Revised December 18, 2002; Accepted January 5, 2003.
Abstract
In systemic lupus erythematosus (SLE) it has been hypothesized that self-reactive B cells arise from virgin B cells that express low-affinity, nonpathogenic germline V genes that are cross-reactive for self and microbial antigens, which convert to high-affinity autoantibodies via somatic hypermutation. The aim of the present study was to determine whether the VH family repertoire and pattern of somatic hypermutation in germinal centre (GC) B cells deviates from normal in SLE. Rearranged immunoglobulin VH genes were cloned and sequenced from GCs of a SLE patient's spleen. From these data the GC V gene repertoire and the pattern of somatic mutation during the proliferation of B-cell clones were determined. The results highlighted a bias in VH5 gene family usage, previously unreported in SLE, and under-representation of the VH1 family, which is expressed in 20–30% of IgM+ B cells of healthy adults and confirmed a defect in negative selection. This is the first study of the splenic GC response in human SLE.
Keywords: spleen, systemic lupus erythematosus
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