ARTHUR F. COCA 1007 



determined the presence of atopic reagins in all of them. He also employed the more 

 delicate method of Dale in seeking to demonstrate passive sensitization in the guinea 

 pigs. The results of Spain's experiments were wholly negative. 



For the present, then, the atopic reagin is identified by its origin in a hypersensi- 

 tive human being; its property of specifically sensitizing the normal human skin; its 

 inability passively to sensitize the guinea pig's uterus; and its inability to render 

 specifically inactive the related atopen. To these outstanding characteristics may be 

 added the minor ones that the atopic reagin is not a precipitin nor a complement- 

 fixing body, and that it is capable, in the passively sensitized skin site, of mediating 

 as many as three successive reactions (wheal and erythema) upon three successive 

 tests with the same quantity of atopen^ — -a peculiarity that is lacking in anaphylactic 

 antibodies.^ 



Bodies capable of specifically sensitizing the human skin have been demonstrated 

 by Rackemann^ and also by Brunner^ in persons that are or that have been harboring 

 intestinal parasites. These bodies have not been studied with respect to the other 

 identifying properties of atopic reagins; but, for the present, they can be separated 

 from the latter by the consideration that the infested individuals do not present any 

 signs of hypersensitiveness to worms. 



Sensitizing reagins are not demonstrable in all cases of human hypersensitiveness, 

 particularly in drug idiosyncrasy^ exhibited to non-antigenic substances, and in some 

 food idiosyncrasies even to antigenic materials. The reagins seem to be consistently 

 absent in the idiosyncrasies that are expressed in urticaria, angioneurotic edema, 

 and gastro-intestinal symptoms, provided asthmatic symptoms are absent. This 

 principle is illustrated in the two cases of sensitiveness to green pea that were studied 

 by Ella F. Grove with the writer.^ One of these subjects presented the symptoms of 

 asthma when green pea was ingested, and exhibited a positive skin reaction to an ex- 

 tract of this vegetable. With the serum of this individual the normal human skin 

 could be locally sensitized to green pea. The second subject suffered no asthma when 

 green pea was ingested, but exhibited angioneurotic edema. The skin test with green 

 pea resulted negatively in this case, and the serum lacked the power of sensitizing the 

 normal human skin. In the considerable group of asthmatics in whom no specific 

 sensitiveness can be demonstrated by means of the skin test, it would seem reasonable 

 to assume that reagins are lacking in the blood. However, the mechanism of the asth- 

 matic attacks in these individuals must, of course, be determined before this question 

 can be finally settled. 



Whether the atopic reagins are true antibodies, i.e., developed immunologically 

 under antigenic stimulation, or physiological products like the natural hemaggluti- 

 nins and hemolysins, is not known. Their increase in the blood during the injections 

 of the excitant (specific treatment) seems to point to an immunological origin. Never- 



' Levine, Philip, and Coca, A. F.: op. cit., 11, 411. 1926; Coca, A. F., and Grove, E. F.: loc. cil. 



2 Coca, A. F., and Grove, E. F.: loc. cil.; Levine, Philip, and Coca, A. F.: op. cit., ir, 411. 1926. 



3 Rackemann, F.: /. Immunol., 13, 389. 1927. 



4 Brunner, M.: read before the American Association of Immunologists, Rochester, N.Y., April 

 15, 1927. /. Immunol., 15. 1928. 



s Coca, A. F., and Grove, E. F.: loc. cil. 



