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Center for Immunology and Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455
Receptor editing is an important mechanism to modify the Ag specificity of newly developing B cells that are reactive with self-Ags. Previous studies have suggested that late immature B cells, bearing high levels of IgM on their cell surface, are unable to initiate receptor editing and instead are deleted by apoptosis. Using the hen egg lysozyme transgenic system, we show that IgMhigh late-immature B cells are fully capable of receptor editing to soluble self-Ag. This was demonstrated by the induction of new endogenous light chain locus rearrangements and by a single-cell flow cytometric assay using a recombination-activating gene 2-green fluorescence protein reporter transgene. These studies suggest that the developmental window available for immature B cells to edit their Ig receptors, at least in response to certain soluble Ags, extends through the IgMhigh late immature B cell stage.
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