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Department of Microbiology and Immunology, Dartmouth Medical School and the Norris Cotton Cancer Center, Lebanon, NH 03756

CORRESPONDENCE Randolph J. Noelle: Randolph.Noelle{at}Dartmouth.edu OR Micah J. Benson: Benson{at}IDI.Harvard.edu

The hypothesis that bystander inflammatory signals promote memory B cell (B_MEM) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 lineage B220⁺IgG⁺ B_MEM toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent B_MEM clonally expand. Surprisingly, proliferating B_MEM do not acquire germinal center (GC) B cell markers before generating daughter B_MEM and differentiating into plasma cells or form structurally identifiable GCs. In striking contrast to cognate antigen, inflammatory stimuli, including Toll-like receptor agonists or bystander T cell activation, fail to induce even low levels of B_MEM proliferation or differentiation in vivo. Under the extreme conditions of adjuvanted protein vaccination or acute viral infection, no detectable bystander proliferation or differentiation of B_MEM occurred. The absence of a B_MEM response to nonspecific inflammatory signals clearly shows that B_MEM proliferation and differentiation is a process tightly controlled by the availability of cognate antigen.

© 2009 Benson et al.
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