The study investigates the mechanism of B cell tolerance in mice transgenic for anti-H-2K^b antibody genes. In these mice, a homogeneous clone of developing B cells can be analyzed for the outcome of autoantigen encounter. The research shows that surface immunoglobulin M^+/idiotype^+ immature B cells binding to self-antigens in the bone marrow are induced to alter the specificity of their antigen receptors through receptor editing. Specifically, transgenic bone marrow B cells encountering membrane-bound K^b or K^k proteins modify their receptors by expressing the V(D)J recombinase activator genes and assembling endogenously encoded immunoglobulin light chain variable genes. This process, termed receptor editing, allows autoreactive B cells to be rescued from elimination by altering the structure and specificity of their antigen receptors. The findings challenge the traditional paradigm of clonal selection, suggesting that receptor editing can uncouple the fates of the autoreactive B cell and its receptor, providing a mechanism for the elimination of potentially harmful autoreactive B cells.The study investigates the mechanism of B cell tolerance in mice transgenic for anti-H-2K^b antibody genes. In these mice, a homogeneous clone of developing B cells can be analyzed for the outcome of autoantigen encounter. The research shows that surface immunoglobulin M^+/idiotype^+ immature B cells binding to self-antigens in the bone marrow are induced to alter the specificity of their antigen receptors through receptor editing. Specifically, transgenic bone marrow B cells encountering membrane-bound K^b or K^k proteins modify their receptors by expressing the V(D)J recombinase activator genes and assembling endogenously encoded immunoglobulin light chain variable genes. This process, termed receptor editing, allows autoreactive B cells to be rescued from elimination by altering the structure and specificity of their antigen receptors. The findings challenge the traditional paradigm of clonal selection, suggesting that receptor editing can uncouple the fates of the autoreactive B cell and its receptor, providing a mechanism for the elimination of potentially harmful autoreactive B cells.