Complement activation and depletion during LDL-apheresis by heparin-induced extracorporeal LDL-precipitation (HELP).

The heparin-induced extracorporeal elimination of low density lipoproteins (LDL) is a well-established clinical procedure to markedly reduce cholesterol levels. The biocompatibility of this artificial filter system (HELP) was investigated by quantitation of representative complement proteins within the extracorporeal circuit using established ELISA procedures, based on monoclonal antibodies recognizing exclusively either native (C6, C7) or activated proteins (act.C3, C5a, TCC).

C7*N is a hypomorphic allele of the human complement c7 M/N protein polymorphism.

Two complement C7 protein polymorphisms exist. One is determined by isoelectric focussing whereas the other is determined by the reaction pattern of a monoclonal C7-allospecific antibody in an ELISA assay. C7 concentrations quantitated by an ELISA based on polyclonal C7-specific IgG and data from functional haemolytic assays were compared with the allotypes of both C7 protein polymorphisms.

C7*9, a new frequent C7 allele detected by an allotype-specific monoclonal antibody.

Two sandwich ELISA for the quantitation of C7 in human plasma--one based on a monoclonal (MAb), the other performed with a polyclonal anti-C7 IgG--were established. Results from ELISA as well as from isoelectric focussing and immunoblotting with both antibodies revealed that the MAb is directed to an allotypic epitope on C7. About 6.