26 FELIX HAUROWITZ 



are formed. We can also take our figures; we don't get such a high ratio, be- 

 cause our antigens are not so efficient as diphtheria toxoid. We get figures of 

 about 10,000 to 100,000 antibody molecules per antigen deposited. 



Chairman Pauling: (Repeating question from audience) Let us suppose 

 that a rat or some such animal has the power of regenerating liver after, per- 

 haps, four-fifths has been removed. Repeating this process, might we investi- 

 gate to see what its antibody production is after this operation? 



Professor Haurowitz: We investigated, in our first experiment, chiefly 

 liver and spleen, but it has been shown by L. L. jMiller in Rochester that the 

 liver does not form antibodies essentially. Most of the antibodies are formed 

 in lymph nodes and in the spleen. You cannot remove all the lymph nodes 

 from the organism. You can remove the spleen, but this will not help because 

 all the lymphatic tissue still remains. Hence this problem cannot be decided 

 experimentally. 



Chairman Pauling: (Repeating question from audience) It was suggested 

 that it might be possible to inject an antigen that destroys itself rapidly, for 

 example, a 100 per cent isotopic antigen, one containing carbon It, say, and 

 that this would be a way of seeing whether destruction of the antigen causes 

 cessation of the antibody formation. 



Professor Haurowitz: I do not think we can prepare any molecule con- 

 taining only C-11 which is at the same time antigenic. I do not know what 

 would happen if such a molecule were injected. 



Chairman Pauling: (Repeating question from audience) What is involved 

 in the binding of complement? 



Dr. Pressman: This is a complicated situation. One possible explanation 

 to which I do not subscribe is that when antigen and antibodies combine there 

 are exposed new sites which now combine complement. However, we also know 

 that antigen and antibodies dissociate. I don't know whether measurements 

 have been made on dissociated antigen or antibody with respect to ability to 

 bind complement, but I presume that neither one alone binds complement. 

 Then any possible new sites which might arise would have to disappear. 



An explanation that appeals to me is the possibility (and it is not original with 

 me) that several antibodies may have a weak intrinsic binding for complement 

 and when several antibody molecules are held closely together by antigen 

 enough complement binding sites would be fixed to hold complement itself 

 very tightly. 



Chairman Pauling: Do you have anything to say. Professor Haurowitz? 



Professor Haurowitz: Complement fixation is rather non-specific and 

 complement is also bound to systems which have nothing to do with antigen- 

 antibody complexes. This complicates matters very much. I think we simply 

 do not know what happens. 



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