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Resting human memory B cells are intrinsically programmed for enhanced survival and responsiveness to diverse stimuli compared to naive B cells


Enhanced secondary Ab responses are a vital component of adaptive immunity, yet little is understood about the intrinsic and extrinsic regulators of naive and memory B cells that result in differences in their responses to Ag. Microarray analysis, together with surface and intracellular phenotyping, revealed that memory B cells have increased expression of members of the TNF receptor, SLAM (signaling lymphocytic activation molecule), B7, and Bcl2 families, as well as the TLR-related molecule CD180 (RP105). Accordingly, memory B cells exhibited enhanced survival, proliferation, and Ig secretion, and they entered division more rapidly than did naive B cells in response to both T cell-dependent and T cell-independent stimuli. Furthermore, both IgM and isotype-switched memory B cells, but not naive B cells, costimulated CD4+ T cells in vitro through a mechanism dependent on their constitutive expression of CD80 and CD86. This study demonstrates that up-regulation of genes involved in activation, costimulation, and survival provides memory B cells with a unique ability to produce enhanced immune responses and contributes to the maintenance of the memory B cell pool.

Type Journal
ISBN 1550-6606 (Electronic)
Authors Good, K. L.; Avery, D. T.; Tangye, S. G.;
Published Date 2009-01-01
Published Volume 182
Published Issue 2
Published Pages 890-901
Status Published in-print
URL link to publisher's version
OpenAccess link to author's accepted manuscript version