B cell development is often portrayed as a series of decision points that expand an antigen-reactive cell to a clone producing a single antibody. This is hardly the case: B cell development is dependent on a series of error-prone, random rearrangement events that through ongoing diversification reach a compromise in which most cells are not autoreactive (except in disease) and the majority of clone members remain specific for the initial antigen. One familiar example of ongoing diversification is somatic mutation during clonal expansion 1. Another example, receptor editing, is the means by which immature bone marrow B cells become self-tolerant 2,3,4. Here rearrangements are induced by encounter with autoantigens to change specificity from self to non-self. Now, a third level of diversification, termed “receptor revision,” has been suggested to occur in mature B...

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