320 GUY A. VOISIN AND RADSLAV KINSKY 



actively against the homologous immunologically competent 

 injected cells or it undergoes passively the consequences of the 

 immunological reactions of the injected cells — but these reactions 

 are peculiar as they do not always lead to runting. Since runting 

 begins very early and already has lethal consequences at a time 

 when the newborn is still incapable of immunological defence one 

 is led to think that — at least for a period of several days after 

 birth — the second possibility is the operative one. What is then 

 the mechanism by which injected cells are prevented from 

 runting the host? One may think that part of the injected 

 cells (presumably stem cells) become tolerant to the host. But 

 this would not prevent the other cells from reacting against the 

 host. One may then invoke a hypothetical process of "exhaustive 

 sensitization" (Simonsen, i960) according to which, when injected 

 cells are sensitized enough to the antigens of the newborn, they 

 are killed by contact with surrounding host antigens, the only 

 surviving cells being the ones which became tolerant. However, 

 if that were so, runting should never happen, owing to the 

 constant overwhelming presence of host antigens. Furthermore 

 it is clear from the present experiments that immunological 

 facilitation protects against runting. If exliaustive sensitization 

 were operative, the reverse would be expected since facilitation, 

 by reducing the quantity of host antigens available to the sen- 

 sitized cells, should decrease the process of exhaustive sensitization. 

 The explanation which seems the most likely to us is that active 

 facilitation of the newborn by the homologous injected cells 

 themselves is the basis for an answer to the problem under con- 

 sideration. It seems now rather well established that immunolo- 

 gically competent cell populations are able to react in two 

 immunological ways to homologous living cells (Snell, 1957^; 

 Medawar, 1959; Mitchison and Dube, 1955): one way being the 

 establishment of a state of delayed hypersensitivity towards 

 transplantation antigens (Brent, Brown and Medawar, 1959) 

 (which may be operative in the rejection reaction) ; the other way 



