The Journal of Experimental Medicine
Geisel School of Medicine
The hypothesis that bystander inflammatory signals promote memory B cell (BMEM) 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 + BMEM toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent BMEM clonally expand. Surprisingly, proliferating BMEM do not acquire germinal center (GC) B cell markers before generating daughter BMEM 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 BMEM 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 BMEM response to non-specific inflammatory signals clearly shows that BMEM proliferation and differentiation is a process tightly controlled by the availability of cognate antigen.
Benson MJ, Elgueta R, Schpero W, Molloy M, Zhang W, Usherwood E, Noelle RJ. Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals. J Exp Med. 2009 Aug 31;206(9):2013-25. doi: 10.1084/jem.20090667. Epub 2009 Aug 24. PMID: 19703988; PMCID: PMC2737154.
Dartmouth Digital Commons Citation
Benson, Micah J.; Elgueta, Raul; Schpero, William; Molloy, Michael; Zhang, Weijun; Usherwood, Edward; and Noelle, Randolph J., "Distinction of the Memory B Cell Response to Cognate Antigen Versus Bystander Inflammatory Signals" (2009). Dartmouth Scholarship. 2649.