Abstract
There are no known specific markers for memory B cells in mice, although studies suggest that the CD38low and CD38high phenotypes are indicative of isotype-switched germinal center (GC) and memory B cells in the mouse, respectively [1]. Further analysis suggested that IgG1+CD38high B cells, but not IgG1+CD38low B cells, are capable of inducing a significant IgG1 secondary response in the adoptive hosts [2], demonstrating that the CD38low and CD38high phenotype distinction can be used to monitor the development of the antigen-specific memory B cells in the T cell-dependent (TD) response. In humans, approximately 30–50% of the peripheral blood B cells are CD27+, and CD27 has been identified as a good surface marker for human memory B cells [3–5]. IgD−CD27+ cells in the peripheral blood have already undergone class switch recombination (CSR) and have accumulated somatic hypermutations (SHMs) in their VH genes in comparison to CD27− B cells, which have not. Polyclonal stimulation of B cells from anthrax vaccine adsorbed (AVA) vaccinated individuals generated AVA-specific IgG+ antibody-secreting cells (ASCs) in vitro, but the deletion of CD27+ B cells abrogated the response [6], indicating that human memory B cells are present in the CD27+ B cell compartment.
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