B cells can revise their antigen receptors outside the confines of the bone
marrow by secondary Ig gene rearrangements. Although the initial motivatio
n to perform these revisions might be to silence a self-reactive specificit
y, those B cells that reinitiate the recombination process can perform a se
ries of 'leaping' rearrangements and inadvertently shift their receptor spe
cificity towards autoimmunity. Heavy-chain receptor revision, coupled with
other atypical rearrangements, might contribute to autoantibody production
in systemic lupus erythematosus.