FIGURE 6.
Model for the regulation of phagocytosis by cross-talk between LTB4-BLT1 and IgG-FcγRs signaling pathways. Binding of IgG-bound pathogens to FcγRs induces cross-linking of FcγRs and subsequent phosphorylation of tyrosine residues in the ITAM of FcRγ by Src family kinases (SFKs). Phosphorylated ITAM then serves as docking sites for the SH2 domain of Syk kinase. Docking of Syk triggers its phosphorylation by SFKs. Syk activation triggers stimulation of PI3K and a GTPase Rac, resulting in an acceleration of phagocytosis. PI3K and Rac also play a pivotal role in phagocytosis downstream of BLT1. LTB4-BLT1 signaling induces both Rac activation through Gi protein and PI3K activation, and these activations lead to an augmentation of phagocytosis.