Figure 7.
Figure 7. Potential models for how LPS signaling is mediated in B lymphocytes. LPS activates B cells through 2 known receptors: RP105 and TLR4. RP105 is B-cell specific while TLR4 is universally expressed, and each used distinct pathways. LPS binding to RP105 induces Lyn activation and CD19 phosphorylation. Phosphorylated CD19 augments Lyn kinase activity and also mediates the Lyn and Vav interaction, which may be crucial for JNK activation. PI 3-kinase and Btk are activated independent of CD19 and regulate [Ca2+]i responses. LPS binding to TLR4 activates MyD88/IRAK and MyD88-independent TIRAP pathways to activate JNK and NFκB.

Potential models for how LPS signaling is mediated in B lymphocytes. LPS activates B cells through 2 known receptors: RP105 and TLR4. RP105 is B-cell specific while TLR4 is universally expressed, and each used distinct pathways. LPS binding to RP105 induces Lyn activation and CD19 phosphorylation. Phosphorylated CD19 augments Lyn kinase activity and also mediates the Lyn and Vav interaction, which may be crucial for JNK activation. PI 3-kinase and Btk are activated independent of CD19 and regulate [Ca2+]i responses. LPS binding to TLR4 activates MyD88/IRAK and MyD88-independent TIRAP pathways to activate JNK and NFκB.

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