Abstract
Following encounters with microbes, cellular activation programs that involve the control of proliferation and survival are initiated in follicular B cells either via the B-cell receptor in a specific antigen-defined manner, or through Toll-like receptors (TLRs) that recognize specific microbial products. This review summarizes and discusses recent findings that shed light on how the nuclear factor kappaB pathway controls and coordinates B-cell division and survival following TLR4 engagement.
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