Abstract
As we have reported a little over a year ago, 1 the interaction between an immune serum and its corresponding substratum is followed by a formation of toxic split products. We found that the toxic material originated not from the substratum or antigen, but from the serum itself. 2 These findings threw light on some of the unsettled questions in the theory of anaphylaxis and antianaphylaxis. Experiments conducted with the view of correlating our findings with the accepted views on this subject, suggested a following hypothesis about the nature and mechanism of anaphylaxis.
Blood serum contains normal proteolytic ferments which require special conditions of the medium in order to exhibit their activity. Normally the degree of concentration of colloids in the serum offers an obstacle to the activity of these ferments. In the experiments in vitro it is possible to change the degree of concentration of colloids in the serum, thus diminishing its antitryptic inhibiting power and setting free the ferments. 3
This activation of normal serum can be accomplished by mechanical adsorption, as in experiments of Plant, Peiper and others, or by the dissolution of some of the serum colloids, as in the experiments of Jobling. 4 In either case the degree of dispersion of remaining colloidal particles is increased and thus ferments are allowed to act.
Our experiments have shown that also the physico-chemical changes following the specific interaction between the antigen and antibody influence the colloidal conditions of the medium in the same manner. 5 Our records show that both stalagmometer and refractometer register the increase of dispersion in the immune serum following the addition of the specific antigen and parallel with it the actual measurements of the antitryptic titer of the serum show a steady diminution of the power of this serum to check the activity of its own proteolytic ferments. 6
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