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Department of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455
Receptor editing in the bone marrow (BM) serves to modify the Ag
receptor specificity of immature self-reactive B cells, while anergy
functionally silences self-reactive clones. Here, we demonstrate that
anergic B cells in hen egg lysozyme Ig (HEL-Ig)/soluble HEL double
transgenic mice show evidence of having undergone receptor editing in
vivo, as demonstrated by the presence of elevated levels of endogenous
light chain rearrangements in the BM and spleen. In an in vitro
IL-7-driven BM culture system, HEL-Ig BM B cells grown in the presence
of soluble HEL down-regulated surface IgM expression and also showed
induction of new endogenous light chain rearrangements. Using a
panel of soluble protein ligands with reduced affinity for the HEL-Ig
receptor, the editing response was shown to correlate in a
dose-dependent fashion with the strength of signaling through the B
cell receptor. The finding that the level of B cell receptor
cross-linking sufficient to induce anergy in B cells is also capable of
engaging the machinery required for receptor editing suggests an
intimate relationship between these two mechanisms in maintaining B
cell tolerance.
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