The study investigates the fate of B cells bearing anti-DNA antibodies in normal mice by generating transgenic mice expressing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. The results show that the transgenic immunoglobulin receptor is not expressed by animals bearing both transgenes, while single transgenic animals (H or L) express their transgenes. Young transgenic animals exhibit reduced B cell numbers, whereas adult animals maintain near-normal B cell counts. Analysis of adult B cells reveals that they use endogenous L chains in association with the transgenic H chain, indicating that the transgenic L chain can be replaced by endogenous L chains. This receptor editing allows autoreactive B cells to escape deletion and maintain their survival. The study suggests that receptor editing, where the L chain is replaced by a nonautoreactive L chain, is a mechanism used by immature autoreactive B cells to avoid tolerance.The study investigates the fate of B cells bearing anti-DNA antibodies in normal mice by generating transgenic mice expressing the heavy (H) and light (L) chain genes of a well-characterized anti-double-stranded DNA antibody. The results show that the transgenic immunoglobulin receptor is not expressed by animals bearing both transgenes, while single transgenic animals (H or L) express their transgenes. Young transgenic animals exhibit reduced B cell numbers, whereas adult animals maintain near-normal B cell counts. Analysis of adult B cells reveals that they use endogenous L chains in association with the transgenic H chain, indicating that the transgenic L chain can be replaced by endogenous L chains. This receptor editing allows autoreactive B cells to escape deletion and maintain their survival. The study suggests that receptor editing, where the L chain is replaced by a nonautoreactive L chain, is a mechanism used by immature autoreactive B cells to avoid tolerance.