Abstract
Activation of complement may result in the generation of the amplification convertase C3bBb. This convertase can be stabilized by properdin (P) or C3NeF. C3bBbP is susceptible to inactivation by beta 1H, while C3bBbNeF is relatively resistant. Since it has been shown that the human erythrocyte C3b receptor (CR1) is able to inactivate C3bBbP, the inactivating action of CR1 on C3bBbNeF was investigated CR1 is at least five times more efficient than beta 1H in inactivating C3bBbNeF. Kinetic studies revealed that CR1 induces an enhanced biphasic kinetics of decay of C3bBbNeF; further purification of this C3NeF preparation by cation exchange chromatography showed that this phenomenon is dependent on the population of C3NeF. Finally CR1 is also able to inactivate fluid phase C3bBbNeF.
MeSH Terms
Complement Activating Enzymes/antagonists & inhibitors,metabolism
Complement C3 Nephritic Factor/immunology
Complement C3-C5 Convertases/antagonists & inhibitors,metabolism
Complement C3b/metabolism
Complement C3b Inactivator Proteins/pharmacology
Complement Factor H
Complement Inactivator Proteins/immunology
Erythrocytes/immunology
Humans
Kinetics
Receptors, Complement/immunology
Time Factors
Chemicals
CFH protein, human
Complement C3 Nephritic Factor
Complement C3b Inactivator Proteins
Complement Inactivator Proteins
Receptors, Complement
Complement C3b
Complement Factor H
Complement Activating Enzymes
Complement C3-C5 Convertases
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Daha M R
Kok D J
Van Es L A
References (18)
18 references, click to expand
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