Receptor editing is a process by which self-reactive B cells in the bone marrow alter their antigen receptor specificity in response to self-antigens. This study shows that in transgenic mice expressing anti-H-2K antibodies, B cells encountering self-antigens in the bone marrow undergo receptor editing by modifying their antigen receptors through secondary light chain gene rearrangement. This process, termed receptor editing, allows autoreactive B cells to avoid elimination by changing their antigen specificity. In B cells, each cell has a unique antigen receptor composed of a single Ig light chain and a single heavy chain. Despite the potential to produce multiple heavy and light chains, allelic exclusion ensures that only one Ig light chain and one heavy chain are expressed. This exclusion is crucial for the high specificity of the B cell receptor, which is essential for clonal selection. In the bone marrow, B cell development involves the rearrangement and expression of Ig genes. Heavy chain gene assembly begins in pro-B cells, followed by light chain gene rearrangement. Light chain rearrangement occurs at the κ locus, while λ light chain rearrangement may represent a salvage pathway. The expression of membrane-bound μ heavy chains mediates allelic exclusion by inhibiting heavy chain gene rearrangement. Autoreactive B cells are continuously produced in primary lymphoid organs. To study negative selection, transgenic mice were used, which express functional Ig genes encoding autoantibodies. These studies suggest that B cells can be tolerized to self-antigens, and multiple mechanisms may be involved in this tolerance. Experiments using transgenic mice showed that autoreactive B cells are selected against through "clonal deletion." Encounter with self-antigens in the bone marrow leads to the elimination of autoreactive B cells from secondary lymphoid tissues. However, a large pool of self-reactive IgM-low B cells remains in the bone marrow, suggesting developmental blockage. This study addresses the mechanism of deletion in B cells reactive to membrane-bound autoantigens. It tests the hypothesis that receptor selection, rather than clonal selection, occurs in immature B cells. Data support this hypothesis, indicating that autoreactive B cells encountering self-antigen attempt and often succeed in altering their specificities through secondary Ig light chain gene rearrangement. The study used transgenic mice and bone marrow chimeras to analyze the effects of self-antigen on B cell development. Elevated RAG-1 and RAG-2 expression was observed in centrally deleting mice, indicating increased light chain gene rearrangement. These results suggest that autoreactive B cells can be rescued from elimination by altering their antigen receptor specificity. The findings highlight the importance of secondary Ig gene rearrangements in B cell tolerance. These rearrangements can create new, functional light or heavy chain genes, effectively changing the antigen specificity of the cells. The study also shows that receptor editing can extinguish the original specificity of B cells, suggesting that autReceptor editing is a process by which self-reactive B cells in the bone marrow alter their antigen receptor specificity in response to self-antigens. This study shows that in transgenic mice expressing anti-H-2K antibodies, B cells encountering self-antigens in the bone marrow undergo receptor editing by modifying their antigen receptors through secondary light chain gene rearrangement. This process, termed receptor editing, allows autoreactive B cells to avoid elimination by changing their antigen specificity. In B cells, each cell has a unique antigen receptor composed of a single Ig light chain and a single heavy chain. Despite the potential to produce multiple heavy and light chains, allelic exclusion ensures that only one Ig light chain and one heavy chain are expressed. This exclusion is crucial for the high specificity of the B cell receptor, which is essential for clonal selection. In the bone marrow, B cell development involves the rearrangement and expression of Ig genes. Heavy chain gene assembly begins in pro-B cells, followed by light chain gene rearrangement. Light chain rearrangement occurs at the κ locus, while λ light chain rearrangement may represent a salvage pathway. The expression of membrane-bound μ heavy chains mediates allelic exclusion by inhibiting heavy chain gene rearrangement. Autoreactive B cells are continuously produced in primary lymphoid organs. To study negative selection, transgenic mice were used, which express functional Ig genes encoding autoantibodies. These studies suggest that B cells can be tolerized to self-antigens, and multiple mechanisms may be involved in this tolerance. Experiments using transgenic mice showed that autoreactive B cells are selected against through "clonal deletion." Encounter with self-antigens in the bone marrow leads to the elimination of autoreactive B cells from secondary lymphoid tissues. However, a large pool of self-reactive IgM-low B cells remains in the bone marrow, suggesting developmental blockage. This study addresses the mechanism of deletion in B cells reactive to membrane-bound autoantigens. It tests the hypothesis that receptor selection, rather than clonal selection, occurs in immature B cells. Data support this hypothesis, indicating that autoreactive B cells encountering self-antigen attempt and often succeed in altering their specificities through secondary Ig light chain gene rearrangement. The study used transgenic mice and bone marrow chimeras to analyze the effects of self-antigen on B cell development. Elevated RAG-1 and RAG-2 expression was observed in centrally deleting mice, indicating increased light chain gene rearrangement. These results suggest that autoreactive B cells can be rescued from elimination by altering their antigen receptor specificity. The findings highlight the importance of secondary Ig gene rearrangements in B cell tolerance. These rearrangements can create new, functional light or heavy chain genes, effectively changing the antigen specificity of the cells. The study also shows that receptor editing can extinguish the original specificity of B cells, suggesting that aut