Figure 2.

Becoming a follicular or a MZ B-cell?. Left panel: Strong signalling through BcR activates Bruton's tyrosine kinase (BTK), which in turn activates the canonical nuclear factor-kB (NF-kB) signalling pathway and prevents the cleavage of Notch2. BAFF-BAFF-R interactions deliver survival signals through NF-KB activation. Right panel: Notch2 can interact with its ligand, Delta-Like 1 (DL1), specifically expressed by the endothelial cells of red pulp venules in mice. This interaction initiates the cleavage of Notch2, which is not inhibited by weak BcR signalling. The intracellular domain of Notch2 enters into the nucleus where it interacts with Mastermind-like 1 (MAML1) and RBP-J transcription factors. This transcriptional complex induces the commitment of B-cells towards MZ B-cells. BAFF-BAFF-R interactions deliver survival signals through canonical NF-KB activation.

Garraud et al. BMC Immunology 2012 13:63   doi:10.1186/1471-2172-13-63
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