Autoreactive B cells may avoid deletion or inactivation by changing the specificity of their immunoglobulin (Ig) antigen receptor. This process is referred to as receptor editing and involves secondary Ig gene rearrangement. For example, in response to encounter with self-antigen, autoreactive B cells may undergo secondary L chain gene rearrangement at their Ig k or l loci and express a different L chain. Knowing when and how receptor editing is initiated is important for understanding B cell differentiation, particularly in the context of autoimmunity. Our studies deal with receptor editing at the Ig heavy (H) and L chain loci in anti-self (DNA) B cells.