MECHANISM OF ANTIBODY FORMATION 103 



change, unlike the changes ensuing from cross-fertilizing genetic 

 changes, is invariably brought about by agents genetically, or species 

 specifically, not related to the cells undergoing this change, and 

 since antigens are foreign to the host undergoing immunization, one 

 may postulate similarities between the action of antigens and muta- 

 genic chemical agents. 



Such a change of degradative nature could be expected to yield 

 mutant cells which, one may assume, produce specific antibodies as 

 abnormal by-products. As in all degradatively produced mutant cells, 

 such a postulated change in host cells would be expected to be of 

 permanent and inheritable character, and would, superficially, support 

 the idea of life-long lasting immunity to certain viruses claimed by 

 Burnet, et al. and implied by their theory. Since, however, immunity 

 to the dominant number of toxic and non-toxic antigens is of temporary 

 nature, one must assume that antibody producing cells or their enzymes 

 do not undergo a degradative mutation preceding or concomitant wdth 

 active immunization. Furthermore, toxic agents which induce muta- 

 tions, are known to suppress or interfere with the metabolism or synthe- 

 sis of specific cell metabolites or components. In contrast, immunity 

 to antigens is accompanied by hyperglobulinemia and not by hypo- 

 globulinemia, indicating that antigens do not suppress the synthesis of 

 globulins. 



Certain antigens produce toxic effects and pathological conditions in 

 a host followed by antibody production or immunity. Non-antigenic 

 drugs or toxic agents also produce noxious effects on cells (for example, 

 inhibition of enzyme activities) resulting in the development of re- 

 sistance to these effects. Unlike the latter effects, certain antigenic 

 toxins, for example, produce their effect functioning as enzymes and 

 destroying the host tissue components, e.g., lecithinase, proteolytic, 

 necrotic and hemolytic actions of bacterial products and snake venoms. 

 However, the host system is not known to develop a non-immune 

 resistance'*' to these toxins in a manner comparable, for example, to 

 the resistance manifested by a bacterium to a drug. Bacterial drug 



*If a resistance in a host can be shown to have resuhed from the action of the 

 toxins of infectious agents, it is not improbable that the action of the toxins, hke 

 those of the antibacterial drugs (Sevag, 1946; Sevag and Gots, 1948; Steers and 

 Sevag, 1949; Sevag and Steers, 1949), have permanently abolished the receptor sites 

 of the host tissues. This would result in a life-long resistance to the toxins of the 

 infectious agents concerned. 



