Figure 7.
Figure 7. Proposed model of NADPHox activation by LTB4. Either binding of IgG-coated targets with the FcγR or ligation of BLT1 by LTB4 results in increased levels of intracellular Ca++ and diacylglycerol (DAG). Ca++ activates cPLA2 activity, which results in enhanced AA release and subsequent generation of LTs. LTB4 stimulates PKC-δ through an unknown mechanism, whereas DAG directly activates this enzyme. Once activated, PKC-δ induces phosphorylation and translocation of p47phox to the plasma membrane, generating ROIs. LTs may also act indirectly by increasing cPLA2 activity (dashed line and question mark).

Proposed model of NADPHox activation by LTB4. Either binding of IgG-coated targets with the FcγR or ligation of BLT1 by LTB4 results in increased levels of intracellular Ca++ and diacylglycerol (DAG). Ca++ activates cPLA2 activity, which results in enhanced AA release and subsequent generation of LTs. LTB4 stimulates PKC-δ through an unknown mechanism, whereas DAG directly activates this enzyme. Once activated, PKC-δ induces phosphorylation and translocation of p47phox to the plasma membrane, generating ROIs. LTs may also act indirectly by increasing cPLA2 activity (dashed line and question mark).

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