FREDERICK P. GAY 883 



explanation of antibody production, has never demonstrated that any particular 

 organ or tissue is responsible for the formation of any given antibody. 



It was quite natural that the scientific world, impressed by the brilliancy of the 

 Ehrlich concept, should expect to find antibody formation in those cells that first fix 

 the antigen and therefore in the leukocytes or the leukocyte-forming organs. We may 

 well question whether phagocytosis and intracellular destruction of a microbe or for- 

 eign red blood cell represent the final fixation of the antigenic proteins of which it is 

 composed. In other words, one should prove the persistence of an antigen or, better 

 still, detect the precocious appearance of the corresponding antibody in a given tissue, 

 in order to demonstrate its antibody-producing function. Experiments in this 

 direction have been contradictory. The work of Deutsch,' Castellani,^ Weil and 

 Braun,^ and particularly of Kraus and Schiffmann^ indicates that agglutinins appear 

 in the serum before they are found in organ extracts. On the other hand, Cantacuzene^ 

 and Swerew^ have noted a hyperleukocytosis preceding the formation of precipitins. 

 Stenstrom^ found that more precipitins are produced on injecting the foreign protein 

 with admixture of the leukocytes of the immunized animal. Pfeiffer and Marx,^ how- 

 ever, found less antibodies in leukocyte extracts than in the plasma. 



Persistent antigens have been sought for by adding organ extracts to a precipitat- 

 ing antiserum. Curiously enough, both precipitinogen and precipitin may concur in 

 the same immune serum.' 



The hematopoietic organs have also been studied as antibody formers. Pfeiffer 

 and Marx found that cholera lysins are present in spleen and bone marrow before 

 they occur elsewhere. The removal of the spleen may or may not lessen antibody 

 formation. Experiments in injuring the leukopoetic organs by benzene or X-rays'*" 

 seem to lower antibody formation in such animals, but the animals are so debilitated 

 by this treatment that one hesitates to draw conclusions. Other authors have im- 

 puted antibody formation to the liver, particularly under stimulation of the iodine 

 content of the thyroid gland." Gay and Rusk' were not able to repeat these experi- 

 ments. Manwaring" and Blaizot have suggested more specifically liver endothelium. 

 Kraus and Schiffman,'^ Eastwood,"" and also Siegmund'^ have attributed antibody 

 formation to the endothelium in general. 



' Deutsch, L.: Ann. de I'lnst. Pasteur, 13, 689. 1899. 



^ Castellani, A.: Ztschr.f. Hyg. u. Infektionskrankh., 37, 381. 1901. 



3 Weil, E., and Braun, H.: Biochem. Ztschr., 17, 337. 1909. 



■• Kraus, R., and Schiffmann, J.: Ann. de Vlnst. Pasteur, 20, 225. 1906. 



s Cantacuzene, J.: ibid., 22, 54. 1908. * Swerew: Russk. Wratsch., 9, Part I, 367. 1910. 



' Stenstrom, O.: Ztschr.f. Immunitdtsforsch. u. exper. Therap., 8, 483. 1911. 



8 Pfeiffer, R., and Marx: Ztschr.f. Hyg. u. Infektionskrankh., 27, 272. 1898. 



9 Gay, F. P., and Rusk, G. Y.: Univ. Calif. Pub. Path., 2, 59. 1912; ibid., p. 73. 1912. 

 '"Rusk, G. Y.: ibid., p. 139. 1914; Simonds, J. P., and Jones, H. M.: /. Med. Research, zi, 183. 



1915- 



"Miiller, L.: Centralbl. f. Bakteriol., Abt. I, Orig., 57, 577. 1911; Fassin, L.: Compt. rend. 

 Soc. de biol., 62, 388, 467, 647. 1907. 



'2 Manwaring, W. H.: Ztschr.f. Immunitdtsforsch. u. exper. Therap., 8, i. 191 1. 



'3 Kraus, R., and Schiffman, J.: Atin. de Vlnst. Pasteur, 20, 225. 1906. 



'4 Eastwood, A.: J. Hyg., 22, 355. 1924. '5 Sicgmund, H.: Klin. Wchnschr., r, 2566. 1922. 



