Abstract

C3 binding glycoprotein (C3bgp) is immunomodulating molecule isolated from the plant Cuscuta europea. When neutrophils were incubated with C3bgp the subsequent binding of anti-CD11b mAb became significantly higher. C3bgp induced moderate TNF-α production in human PBMC and primary monocytes. This production was significantly inhibited by the specific inhibitors of JNK and p38 MAPKs. The inhibition of JNK reduced PBMC viability. We concluded that: (i) C3bgp utilized CD11b polypeptide chain of CR3 and mediated a part of its immunomodulatory properties by activation of JNK and p38 and (ii) PBMC viability at in vitro conditions depends of JNK signal transduction pathway activation.

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