Publication | Closed Access
C3 Shunt Activation in Human Serum Chelated with EGTA
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References
1972
Year
E. ColiImmunologyEscherichia ColiEgta SerumCellular PhysiologyInflammationCell SignalingMolecular PhysiologyBiochemistryReceptor (Biochemistry)C3 Shunt ActivationAutoimmunityImmune FunctionPharmacologyComplement SystemSignal TransductionTherapeutic EfficacyImmunosuppressionMedicine
Abstract Complement (C) fixation via the C3 shunt, as exemplified by zymosan (Z) and Escherichia coli (E. coli), requires ionized magnesium but not ionized calcium and proceeds in the presence of 10 mM ethyleneglycoltetraacetic acid (EGTA). C-fixation via the C142 pathway requires calcium and is inhibited by EGTA. Both pathways of C-activation are inhibited by ethylenediaminetetraacetic acid (EDTA). EGTA serum may be a useful and simple reagent to distinguish between C142 and C3 shunt-mediated complement activation.