THE ORIGIN OF ANTITOXIN THE SIDE-CHAIN THEORY 105 



capable of assimilation by the protoplasm to which it is anchored ; 

 it is not necessary that there should be a toxophore group which 

 injures the cell. In this case the production of the antibody will 

 not be accompanied by any symptoms of disease. The proto- 

 plasmic molecule will have some of its receptors occupied and 

 rendered useless by the foreign proteid, and will have to regenerate 

 others of the same nature, but it will not be injured in any way in 

 the process. It is in this way that we explain the formation of 

 antitoxins as a sequence to the injection of toxoids which have 

 retained their haptophore groups, but lost their toxophores, as 

 well as the formation of agglutinins (to non-pathogenic bacteria), 

 precipitins, etc. 



We pass on to another question that of specificity. We have 

 seen that the antitoxins are, in general, adapted only to neutralize 

 the toxins which lead to their production. To this rule there are 

 a few exceptions, real or apparent. Thus, antirobin serum has 

 also an action against ricin, tetanus antitoxin has apparently 

 some action on snake-venom, anti-snake venom serum neutralizes 

 scorpion venom, etc. The explanation is doubtless that the 

 venoms in question have haptophore groups which closely re- 

 semble one another in their chemical affinities, whilst differing 

 from those of other toxins. Thus, Ehrlich has suggested that 

 robin is the toxon of ricin, in which case the combining portions 

 of the molecules of the two would be identical. 



In any case, the side-chain theory seems to fit quite well with 

 ascertained facts. It explains the specificity ; it is the receptors 

 which unite with the injected toxin which are produced in excess, 

 and which therefore form antitoxin. But in the complex changes 

 in metabolism which must take place in the poisoned cell it is 

 quite easy to imagine that, under certain circumstances, other 

 receptors may either be formed in slight excess as a result of the 

 general stimulation of the cell, or may be cast off in slight excess 

 as a result of necrotic or autolytic processes taking place therein. 

 This may be the explanation of some of the apparent exceptions, 

 especially of those in which the serum has but slight antitoxic 

 power on the toxin which was not injected, whereas it is much 

 more potent on that which was. 



The next question, and a much more difficult and important 

 one, deals with the site of production of the antibodies. Ehrlich's 

 original idea was that the antitoxins are produced from those cells 

 on which the toxins act i.e., on the susceptible cells. For instance, 



