| First Author | Takahashi Y | Year | 2005 |
| Journal | Immunity | Volume | 23 |
| Issue | 2 | Pages | 127-38 |
| PubMed ID | 16111632 | Mgi Jnum | J:100532 |
| Mgi Id | MGI:3588809 | Doi | 10.1016/j.immuni.2005.06.010 |
| Citation | Takahashi Y, et al. (2005) Novel role of the Ras cascade in memory B cell response. Immunity 23(2):127-38 |
| abstractText | 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 naive 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. |
