EHRLICH'S SIDE-CHAIN THEORY 493 



upon the combining affinity of the toxin for certain of the cells 

 of the body, and this again is referred back to the complicated 

 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 

 off. The question, however, arises whether there may not be really 

 an increased resistance of the cells to the toxophorous affinities. 

 An observation recently made by Meyer and Ransom (v. p. 383) 

 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 immun- 

 ised 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 antitoxin 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 contains a large amount of anti- 

 toxin, 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 supersensitiveness 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 toxophorous action in the process of immunisation an 

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

 freshly introduced toxin may reach the cells in spite of the anti- 



