59 



resistant, and the naturally immune animal are only differences 

 in degree. The explanation, then, would be that in the naturally 

 immune animal the interchange of bodily activities, termed 

 metabolism, is unfavourable to the multiplication of the bacterium 

 in question because these activities are balanced in such a way 

 that none of the interacting colloids are free to inhibit antibacterial 

 action. The serum of such an animal need not be bactericidal 

 in vitro and need not be protective, in ordinary doses, because the 

 interacting forces between which the equilibrium exists are 

 only active in the living body and are not represented in the 

 serum. In the susceptible and normal animal, it is to be supposed 

 that, when the bacterium is introduced, there is some " buffer 

 action " which tends to inhibit the animal's natural antibacterial 

 forces; the result of the infection will depend on the degree of 

 this intervention, being in favour of the bacteria if the inter- 

 ference is great and in favour of the animal if it is too small to 

 be permanently effective. When an animal, originally sus- 

 ceptible, has acquired active immunity, it is to be assumed that 

 immunisation has produced a new equilibrium, which has been 

 adjusted in accordance with the influence of the immunising 

 antigen and has eliminated the " buffer action " for that 

 particular bacterial type. This condition of active immunity 

 need not be accompanied by demonstrable antibodies, and, for 

 the same reasons which applied to the naturally immune animal, 

 the serum may not be bactericidal in vitro and may not confer 

 passive immunity. 



It appears to me that attempts, such as the above, to apply 

 ideas of a balanced mechanism to problems of immunity are 

 not substantial enough to carry conviction. They are obviously 

 not intended as an alternative explanation in cases where the 

 immunological data are fairly simple. For example, there is a 

 recognised association between resistance to diphtheria and the 

 presence of antitoxin in the serum ; this is a concrete fact which 

 goes a long way towards explaining immunity against that 

 disease, though it may not be the complete explanation. And 

 there are many other well known instances where susceptibility 

 or resistance to infection is correlated with the presence or 

 absence of demonstrable antibodies. In such cases, theories about 

 equilibrium would not serve any useful purpose. But in other 

 and more obscure cases, where immunity cannot be shown to be 

 due to an appropriate antibody and where no substantial or 

 convincing explanation is forthcoming, speculation is desirable 

 and hypotheses about equilibrium are one of the subjects which 

 is entitled to some consideration. Such matters may at least 

 serve to raise the question, which I discuss in the next section, 

 whether there is not a danger of placing too much reliance 

 on individual antigens and antibodies as explanatory of immunity. 



Possible Limitations of the Antigen-antibody Conception. 



It is probable that, in addition to the known types of anti- 

 bodies, such as precipitins, agglutinins, antitoxins, bacterio- 



