B Cell Receptor (BCR) Cross-Talk: CD40 Engagement Enhances BCR-Induced ERK Activation

摘要: Bystander B cells may be initially stimulated through CD40, which enhances susceptibility to Fas-mediated apoptosis, before encountering Ag, produces Fas resistance. A key issue in this process is what extent CD40 cross-talk might affect subsequent BCR signaling. It has previously been shown that engagement bypasses or mitigates the need for Bruton's tyrosine kinase signaling NF-kappaB activation. However, full of effects on not delineated. In present study we evaluated possibility CD40-mediated also affects another principal outcome signaling: MAPK We found prior stimulation primary murine with CD40L markedly enhanced level ERK and JNK (but p38 MAPK) phosphorylation produced by subsequently added anti-Ig Ab, much, but all, enhancement was independent PI3K phospholipase C. treatment similarly BCR-induced (MEK) phosphorylation, MEK required ERK. Although c-Raf treatment, MEK/ERK phosphorylation. These results identify a novel system receptor between indicate spread beyond involve pathway.