THEORIES OF IMMUNITY 151 



cells without stimulating the production of antibodies, as otherwise 

 the food would be attacked by cast-off receptors and rendered useless 

 before it reaches cells, the process ending in starvation and death. 



The host in whom certain cells with special receptors for a given 

 poison are present will make use of these, no matter how the pathologic 

 agent is introduced. This affinity is well illustrated in tetanus, where 

 the effects produced are dependent to a large extent upon the selective 

 affinity of the toxin for nerve-cells. 



THE THREE ORDERS OF RECEPTORS AND CORRESPONDING ANTIBODIES 



First Order: Antitoxin and Simple Antiferments. The simplest 

 receptor of the cell molecule is composed of a single arm or haptophore, 

 for union with the haptophore portion of a food molecule. As previously 

 stated, a molecule of toxin is conceived as being composed of two por- 

 tions one, the haptophore, for union with the side-arm or receptor of a 

 cell molecule, and the second, the toxophore, in which its toxic action 

 resides. 



The first stage of intoxication of a cell produced by a true toxin 

 consists in the union of the haptophore portion of the toxin molecule 

 to a receptor or side-arm of the cell molecule, this receptor being one 

 that fits the toxin molecule "like a key fits a lock." Each molecule of 

 the body-cell has innumerable receptors, of which only a certain number 

 are suitable for a particular toxin. The toxin molecule is now anchored 

 to the living cell, and, as animal experiments with a great number of 

 toxins show, this union is a firm and enduring one (Fig. 39). 



So long as the union lasts the side-chain involved cannot exercise its 

 normal nutritive physiologic function the taking up of food-stuffs. 

 Furthermore, the toxophore group of the toxin molecule may now exert 

 an injurious, enzyme-like action on the protoplasm of the cell, with the 

 result that the protoplasm is poisoned. If only a few of the cell receptors 

 are united with toxin molecules, or if the toxin is of low toxicity, the 

 effects on the cell may be slight. If more are joined to the molecule 

 or the toxin is highly poisonous, the whole molecule, and finally the cell 

 itself, may be greatly disturbed, and produce marked symptoms, or the 

 host may be destroyed. 



Since the receptors joined to the toxin molecules are incapacitated 

 or destroyed, the damage is repaired by the regeneration of new recep- 

 tors. According to the reparative principles worked out by'Weigert, 

 the repair is not a simple replacement of the defect the compensation 

 proceeds far beyond the necessary limit; indeed, overcompensation is 



