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Antigen-experienced IgM(+) B cells with mutated V genes have emerged as important effectors of both adaptive and innate-like immune responses. While their precise role in recall responses appear to differ according to the nature of the immunogen or the infectious agent, they are able to achieve rapid plasma cell differentiation, germinal center re-initiation, as well as IgM and IgG memory pool replenishment, which establishes them as multi-lineage precursors of the various functional memory subsets. For innate-like responses, recent data have shown that activation by gut commensals is able to generate, both in mice and humans, a systemic IgM(+) population with specificity against glycan epitopes, which displays broad cross-reactivity towards multiple micro-organisms, and ensures a first line of defense against systemic infections.

Post-rearrangement diversification of the antibody repertoire relies on a DNA editing factor, the cytidine deaminase AID. How B lymphocytes avoid generalized mutagenesis while expressing high levels of AID remained a long-standing question. Genome-wide studies of AID targeting combined to the discovery of several co-factors controlling its recruitment and its local activity shed new light on this enigma.

Studies of the immune system of various species have revealed that antibody repertoire can be generated in many different ways. This review underlines some general principles for comparing the different processes which represent the basic framework of these systems.