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Immunity. 2005 Aug;23(2):127-38.

Novel role of the Ras cascade in memory B cell response.

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Department of Immunology, National Institute of Infectious Diseases, Shinjuku, Tokyo, Japan.


Engagement of the B cell antigen receptor (BCR) triggers the Ras cascade, but the biological role of the latter in B cell response is unknown. Here, we report that in T cell-dependent response, the role of the Ras cascade is confined to memory B cells and possibly marginal zone B cells. When Ras-dependent BCR signaling was impaired, the generation of IgG germinal center B cells was unaffected but the recruitment of high-affinity cells into the memory compartment and terminal differentiation were inhibited. Furthermore, inhibition of MEK activity consistently impaired antibody production by IgG memory B cells (but not naïve B cells) in vitro. Notably, this impairment was countered by overexpression of Bcl-2. Thus, our data suggest that upon antigen stimulation, memory B cells are susceptible to apoptosis but can be rescued via an antiapoptotic effect mediated through the Ras cascade.

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