202 INFECTION AND IMMUNITY. 



(perhaps on the "Leistungskern") . The more 

 toxin introduced, the greater the number of cell 

 receptors bound, and the greater the injury to the 

 cell. 



In case a non - fata l amount of toxin has been 

 bound, but sufficient to cause some injury, how 

 does the cell respond to the injury? Weigert, a 

 few years ago, gave expression to a hypothesis 

 which is held to have some bearing on this ques- 

 tion. In studying regeneration following injury 

 he concluded that tissues have the tendency to 

 reproduce not only to the extent of making good 

 the injury, but that an excess of new tissue re- 

 sults. The clearest example of this occurrence is 

 that of scar formation, in which a seeming excess 

 of new connective tissue cells is formed, 

 which later disappears in part. Similarly, when 

 a non-fatal amount of toxin unites with the 

 receptors, a cell defect or injury is created. The 

 cell has for practical purposes lost so many recep- 

 tors. This loss affects the vital activities of the 

 cell, the "Leistungskern" and new receptors, iden- 

 tical with those occupied, are reproduced. Follow- 

 ing the law stated, they are reproduced in excess 

 of the number injured, and the excess may be so 

 great that the cell may be overfilled with them 

 so overfilled that many are discharged and reach 

 the general circulation. These cast-off receptors, 

 or side-chains, still retaining their power of unit- 

 ing with toxin, constitute our antitoxins. As 

 Behring has stated it, the receptor, when attached 

 to the cell, is the agent through which the latter 

 is attacked, but when cast off from the cell becomes 

 its protector (Fig. 5). 



