IMMUNOLOGY 861 



Thereafter it is not adequately augmented and supplemented by an active 

 ablastic immunity in splenectomized and blockaded animals, as it is in 

 normal rats, because the active immunity is slow in developing and 

 decreased in amount. Splenectomy and blockade definitely decrease the 

 effectiveness of the trypanolysins. It would seem that such an effect 

 could be adequately explained by a decrease in the amount of comple- 

 ment which would prevent the lysis of sensitized trypanosomes, or by a 

 decrease of macrophages which would prevent the removal of opsonized 

 parasites. The fact that previously sensitized trypanosomes are as readily 

 removed in splenectomized and blockaded animals as in normal rats 

 seems to negate both of these suppositions, unless the sensitized trypano- 

 somes are agglutinated and removed mechanically — a possibility which 

 because of technical difficulties has not yet been ruled out. A more likely 

 explanation is that there is an interference with the union of antigen 

 and antibody. 



It has already been indicated that a lysin differs from an opsonin only 

 in that the terminal lysis and death of sensitized organisms may be 

 effected by extra- rather than intracellular enzymes. Just as in the 

 indirect studies discussed in the preceding paragraph, however, direct 

 studies on phagocytosis have failed to indicate whether phagocytosis or 

 lysis is more important in acquired immunity. Laveran and Mesnil 

 (1901) considered that the parasites are actively phagocytosed, and 

 Roudsky (1911) and Delanoe (1912), studying the acquired immunity 

 of mice to T. leivisi, came to the same conclusion. Regendanz and Kikuth 

 (1927) believed that the parasites are phagocytosed in a nonspecific 

 way. MacNeal (1904), Manteufel (1909), W. H. Tahaferro (1924), 

 and Coventry (1929), on the other hand, considered that they are lysed. 

 In studying the tissues for evidence of phagocytosis, we are handicapped 

 by the fact that no easily recognizable vestiges of trypanosomes, such as 

 malarial pigment, remain in macrophages for any appreciable length of 

 time. The fact that pigment by itself may be phagocytosed does not 

 invalidate this statement, since the whole complex, consisting of red 

 cell, parasite, and pigment, is often recognized intact in macrophages. 



To sum up: acquired immunity against nonpathogenic trypanosomes 

 primarily involves ablastin and trypanolysins, the first of which prevents 

 the trypanosomes from undergoing growth and cell division, and the 

 second of which kill the trypanosomes. They are both humoral anti- 



