PROTEIN SENSITIZATION OR ANAPHYLAXIS 325 



highly susceptible, and on the second injection the protein 

 is firmly anchored to the cell, just as the cells of an animal 

 susceptible to tetanus anchor the tetanus toxin. The only 

 difference is that in the latter instance the receptors are 

 preformed, while in the case of sensitization they are 

 developed as a result of the first injection. It is, as Ehrlich's 

 theory explains, the same substance, the receptor, so long as 

 it remains attached to the cell, that is the cause of the 

 poisoning, and which becomes the cause of cure when 

 detached from the cell, and cast off into the blood. The 

 only difference, as has been stated, is that the substance 

 attached to the cell (the receptor) is not, at least in sufficient 

 quantity, preformed, and must be developed by the first 

 injection. Protein (toxin) immunity and anaphylaxis, 

 therefore, are alike save in the proportion and location of 

 the antibodies. When the precipitin is already in the body 

 fluids the injection of the homologous protein is without 

 effect; when the precipitin is still attached to the cell in 

 sufficient quantity the reinjection of the homologous protein 

 is followed by the phenomena of anaphylaxis. The anti- 

 bodies exist in two places: (1) As free antibodies in the 

 serum (known as precipitins in test-tube experiments). 

 (2) As sessile antibodies attached to the cells. In cases of 

 local sensitization, as in Arthus phenomenon, the local 

 cells only are affected because they are the only ones which 

 bear the sessile receptors. The animal escapes anaphyl- 

 actic shock because the cells of the body as a whole, and 

 especially those of the nervous system, do not carry the 

 specific sessile receptors. Friedberger, in his theory, explains 

 antianaphylaxis as follows: An animal is rendered anti- 

 anaphy lactic when it receives a large reinjection before 

 the period of incubation is complete. In this case the 

 reinjection uses up the sessile receptors already developed, 

 but these are not enough to lead to anaphylactic shock, 

 and at the end of the period of incubation the new crop of 

 sessile receptors is not sufficiently developed to give rise 

 to the symptoms of anaphylaxis. Again, an anaphylactized 

 animal may be rendered antianaphy lactic by a small dose 



