58 INTRODUCTION TO IMAIUNOCHEMICAL SPECIFICITY 



carefully from the Ss gene pair which controls the secreting phe- 

 nomenon in the ABO system) are fairly common nearly everywhere 

 and add greatly to the anthropological usefulness of the system. 

 Two others, called Hunter and Henshaw after the donors in whom 

 they were first found, are not too common in Africans and are 

 virtually unknown in persons of European descent. 



Distribution of M and N in the Body 



Boyd and Boyd (1934) were not able to demonstrate M and N 

 in human tissues with the technique which they had devised for 

 A and B. Kosyakov and Tribulev (1939, see also Kosyakov 1954) 

 devised a method by which M and N could be demonstrated. Their 

 work was confirmed by Boorman and Dodd (1943). Whereas Boyd 

 and Tayian (1935) could not detect M and N in boiled erythrocytes, 

 Kosyakov (1954) was able to do so, and also showed these antigens 

 to be heat stable. 



Rh Groups 



In 1939. Levine and Stetson reported a case of erythroblastosis 

 fetalis and ascribed this disease of the newborn to sensitization of 

 the mother to a blood antigen the fetus had inherited from the 

 father. It is now known that this proposed explanation of the disease 

 is correct and that the antigen operating in the case described was 

 one of those now known as Rh. Levine and Stetson, however, did 

 not propose any name for the new blood factor (on such a slender 

 hair sometimes dangles the apple of priority). It was not until 

 Landsteiner and Wiener (1940) discovered that serum from one of 

 their rabbits immunized with rhesus erythrocytes detected a new 

 factor in human blood that the term Rh was introduced. The new 

 factor still might not have attracted any more attention than had 

 others previously reported had not Wiener and Peters (1940) shown 

 that certain transfusion reactions were due to sensitization to Rh 

 and Levine et al. (1941) shown that Rh incompatibility between 

 mother and fetus could be the cause of erythroblastosis fetalis. 



Reduced to the simplest terms, the way Rh incompatibility can 

 cause erythroblastosis fetalis is apparently this : The mother is Rh- 

 negative, and the fetus inherits the Rh blood factor from his father. 



