This section is from the book "Research In Physiopathology As Basis Of Guided Chemotherapy With Special Application To Cancer", by Emanuel Revici. Also available from amazon: Research In Physiopathology
The first group of antibodies have a characteristic property. Together with the antigen, on which they fix with a degree of specificity, they form highly energetic complexes. This is manifest in a marked tendency to bind together such complexes as well as constituents of the blood and form huge aggregates. When such antibodies are produced for, and act against, a specific microbe, agglutination results. Conglutination, precipitation and flocculation occur when similar antibodies act against other antigens. Due to their tendency to establish antigen antibody complexes resulting in huge formations, these antibodies are generally grouped as coagulant antibodies. Although the coagulation characteristic is not demonstrable in vitro for all antibodies in this group, we use the term "coagulant antibodies" for didactic purposes.
The huge complex formation resulting from the binding of coagulant antibodies with an antigen can appear as a precipitate, agglutinated microbe or conglutinated red cells. Once established, this formation represents a new heterogeneous entity of much larger dimensions than the antigen alone. As such, it becomes by itself a new noxious agent for the organism which consequendy reacts against it. The organism utilizes the same processes against this noxious antigen coagulant antibody complex as it uses for any heterogeneous agent, with the same immediate diphasic or prolonged mechanism.
Teleologically, the formation of coagulant antibodies can be interpreted as an attempt of the organism to defend itself anew against the antigen. The antigen, this time fixed through these antibodies in a new and more noxious formation, will once again incite the nonspecific defense mechanism. First there will be the antiheterogeneous response with its diphasic phenomenon and, if once more this is not effective, a prolonged new lipidic intervention will follow. If the quantity of heterogeneous formations is great, the first phase of the diphasic phenomenon can be so severe as to cause death in a few minutes. If less severe, this first phase is followed by the second, with chills and high temperature. As in all the antiheterogeneous reactions, the organism tries to combat the presence of the noxious factor—in this case, the flocculate produced by the antigen antibody bond —attempting to digest it through hydrolytic enzymes or to neutralize it through constituents brought in during the second phase of the diphasic phenomenon. If it fails, the abnormal prolonged form of this response follows with characteristic lipidic liberation.
In terms of biological meaning, the formation of coagulant antibodies represents a new chance for the organism to resume the fight against antigens by using the same fundamental means, the antiheterogeneous reaction. However, since the new agent, the antigen antibody complex, is much more noxious than the antigen alone, the intensity of the response will be much stronger and the chances of disposing of the antigen will be greater.