122 M. HASEK ET AL. 



70-3 per cent. In the case of negative controls the survival was 

 84*6 per cent, v^hereas following injections of other embryonic 

 tissues, strong transplantation immunity was found; survival of 

 the epitheUum of the test skin graft reached only 5 • 5 per cent on 

 the average. After transfer of the placentas into the recipients of 

 the male strain (Table II), the mean survival of the epithelium was 

 26*8 per cent, which meant a good immunity; in negative 

 controls 95*6 per cent; and in positive ones 6-2 per cent follow- 

 ing injections of embryonic tissues. It appeared that neither the 

 age of placentas and embryos, nor the interval between the 

 injection and the test graft affected the results. 



It can be considered that the incapacity of the foetal part of the 

 placenta to induce transplantation immunity might be related to 

 the occurrence of haploid nuclei in syncytiotrophoblast containing 

 perhaps only the mother's set of chromosomes, as assumed by 

 Galton (i960), or that it could be the outcome of a reduced num- 

 ber of transplantation antigens during a rapid development of 

 syncytiotrophoblast or of some other type of phenotypic variation 

 in distribution of transplantation antigens. 



The antigenic inferiority of the placenta demonstrated by the 

 absence of antigens of the mating male in the foetal part of the 

 placenta could throw a hght on why transplantation reaction does 

 not occur at the site of contact of the tissues of foetus and mother. 

 There are, however, cases in which the placental barrier fails. 

 Indirect evidence for such a leakage could be provided either by 

 the occurrence of tolerance in the offspring towards the mother 

 or by the occurrence of immunity in the mother. The occurrence 

 of a spontaneous transplacentally induced tolerance in the mother 

 seems to be very rare (Billingham, Brent and Medawar, 1956; 

 Peer, Walia and Pullen, i960; Rogers, 1958; Owen et al, 1954; 

 Ward, Walsh and Kooptzoff, 1957); it could, however, be 

 artificially increased under appropriate experimental conditions 

 (Lengerova, 1957; Nathan, Gonzales and Miller, i960), probably 

 by the failure of the normal function of the placenta. As far 



