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The immunomodulatory activity of C3 binding glycoprotein (C3bgp) is mediated by the complement receptor type III and mitogen-activated protein kinase signal transduction pathways.

Research paper by Zlatka Georgieva ZG Dobreva, Spaska Angelova SA Stanilova

Indexed on: 14 Dec '07Published on: 14 Dec '07Published in: Immunopharmacology and immunotoxicology



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-alpha 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.