EHRLICH'S SIDE-CHAIN THEORY 551 



constitution of living protoplasm. Furthermore, the^ biological 

 principle involved is no new one, being simply that of over- 

 regeneration after loss. It would appear likely that the integrity 

 of the executive centres of the protoplasm molecules would be 

 essential to the satisfactory production of side-chains, and this 

 would appear in accordance with the fact that antitoxin 

 formation occurs most satisfactorily when there is no marked 

 disturbance of the health of the animal. 



It is to be noted, however, that it does not explain active 

 immunity apart from the presence of anti-substances in the 

 serum. For example, an animal may be able to withstand a 

 much larger amount of toxin than could be neutralised by the 

 total amount of antitoxin in its serum. This might theoretically 

 be explained by supposing a special looseness of the cell re- 

 ceptors so that the toxin-receptor combination became readily cast 

 oft'. The question, however, arises whether there may not be 

 really an increased resistance of the cells to the toxophorous 

 affinities. An observation made by Meyer and Ransom (vide 

 p. 427) is also difficult of explanation, according to the view 

 that antitoxin is formed by the cells with which the toxin 

 combines and on which it acts. They found that in an animal 

 actively immunised against tetanus and with antitoxin beginning 

 to appear in its blood, the injection of a single M.L.D. of 

 tetanus toxin into a peripheral nerve brought about tetanus 

 with a fatal result. On the other hand, the injection of anti- 

 toxin into the sciatic nerve above the point of injection of toxin 

 prevented the latter from reaching the cells of the cord. One 

 can scarcely imagine an explanation of these facts if antitoxin 

 molecules were in process of being shed off by the cells of the 

 nervous system. Further, when the serum of an animal con- 

 tains a large amount of antitoxin, how does the additional 

 toxin injected reach the cells in order to influence them as 

 we know it does'? This also is difficult to understand, unless 

 the toxin has a greater affinity for the receptors in the cells 

 than for the free receptors (antitoxin) in the serum. A super- 

 sensitiveness of the nerve-cells of an animal to tetanus toxin, 

 sometimes observed even when there is a large amount of 

 antitoxin in the serum, has been often brought forward as an 

 objection. But this also may perhaps be explained by there 

 having occurred a partial damage of the cell protoplasm 

 by the toxic action in the process of immunisation an 

 explanation which, of course, demands that in some way the 

 fiv-hly introduced toxin may reach the cells in spite of the anti- 

 toxin in the blood, or it may belong to the group of anaphy lactic 



