Abstract
Two hypotheses were recently presented for the explanation of the mechanism of zoning occurring in complement fixation—one by Levine, 1 the other by Eagle. 2 The two hypotheses rest on principles which possess no element in common. Therefore, I undertook a critical study of the subject matter. In this paper are presented in brief the results of the study of the theory of Eagle.
The latter can be briefly summarized as follows: Serum in concentrations greater than 1:25 effects an inhibition of complement fixation through the adsorption of fixation-preventing substances presumably present in negative serum. 3 These inhibiting substances are adsorbed by the antigen-antibody complexes after they had become fully organized. The adsorption is more intense the more negative a serum is, and corresponds roughly to the concentration of the serum protein. Hence, in weakly positive serums a more pronounced fixation of complement will occur in the higher serum dilution, and hence, the zone phenomenon. This same inhibition, Eagle states, is less marked at lower temperatures, and hence, in an indirect manner it is also responsible for the greater sensitivity of the icebox test.
Experimental studies were carried out as follows: (1) Complement and amboceptor titrations in the presence of high concentrations of negative serum; (2) complement fixation tests with Kahn antigen precipitated from positive and negative reactions 4 in the presence of high negative serum concentrations; (3) the effect of the removal of the native antisheep amboceptor from negative serum and the bearing of this procedure on the assumption that the results of Eagle's original experiments were influenced by natural amboceptor.
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