ANAPHYLAXIS 141 



This result, as I have already shown, is explained on the basis of 

 an acquired receptoric atrophy, and we can readily conceive that this 

 should occur, if the specific receptors which the cell forms under 

 the stimulus of the toxin are continuously cast off, and thus no longer 

 serve a useful purpose so far as the nutrition of the cell is concerned. 

 On the other hand, the opposite may occur. The animal, while 

 actively forming antitoxin, loses its increased resistance to the corre- 

 sponding toxin, and succumbs to a much smaller dose of the latter 

 than the original minimal fatal dose. It is thus no longer immune, 

 but actually hypersensitive. As this phenomenon is only observed 

 in actively and never in passively immunized animals, the conclusion 

 suggests itself that its basis must be histogenetic and not humoral 

 in character. Since antitoxin is present in the blood of the animals 

 in large amount we must suppose that this actually anchors the toxin, 

 but as the animal dies with typical toxin symptoms we must also 

 conclude that the toxin-antitoxin combination is again severed and 

 that the toxin after all reaches the corresponding receptors of the 

 susceptible cells. This, of course, would presuppose the existence 

 of a higher affinity for the toxin on the part of the sessile than of 

 the circulating receptors. That there is actually a basis for such 

 an assumption has been shown by Muller, who could demonstrate 

 that at any one time the blood serum of an animal undergoing 

 immunization contains antibodies of varying degrees of affinity for 

 the corresponding antigen, and that those possessing the highest 

 affinity are the latest formed. 



The hypersusceptibility of the highly immunized animal would 

 thus find a ready explanation, which would also seem to apply in 

 the case of the so-called paradox of Kretz. This investigator found 

 that while the injection of an accurately neutralized toxin-antitoxin 

 mixture produced no deleterious results whatever in the normal 

 animal, in one which had been previously actively immunized with 

 toxin the reverse occurred. Here also we may suppose that as the 

 result of the immunization, highly active receptors are present in 

 the susceptible cells, and that these are capable of displacing the 

 antitoxin which had been added in vitro and of anchoring the liberated 

 toxin which then acts upon the cell before this has cast off the cor- 

 responding receptors. 



If coincidently in either one of the two instances just considered 

 receptoric atrophy should develop in the non-susceptible cells it is 



