On the Blood Group Antigens Bua and Sm MARION LEWIS, BRUCE CHOWN AND HIROKO KAITA

From the Department of Pediatrics, University of Manitoba, and Rh Laboratory, Winnipeg, Manitoba, Canada

Three Bu(a+)Sm+ x Bu(a+)Sm+ famifiea with three Bu(a+)Sm-, 11 Bu(a+)Sm+ and seven Bu(a-)Sm+ children are reported, support- ing the hypothesis that Bua and Sm are products of allelic genes. The inheritance of Bua has been shown to be independent of sex and of all blood group systems reported prior to 1962 except Diego, Yt and Auberger. It is now reported to be inde pendent of the antigens D o a and Cs*.

THE DATA PRESENTED HERE support our earlier proposition4 that the blood group antigens Bua and Sm may be products of allelic genes. The discovery of new exam- ples of anti-Bua by Seyfried, Frankowska and Giles6 and the generous gift of a quan- tity of the best of these, Soch, by Dr. Sey- fried, have made it possible to gather the data.

The frequencies of Bu (a+) in reported Caucasian samples differ widely: 1 in l,OOO;4 9 in 1,025 and 7 in 1,039;6 5 in 848.3 In this last sample three of the five Bu(a+) were local Mennonites, which suggested that Bua, and hence informative mating types, might be more frequent among them than in the general population. Accord- ingly, blood samples from 200 young Men- nonites applying for marriage licenses were tested for Bua: seven were positive. Five of the seven proved to belong to one large and somewhat inbred kindred. The kindred had a printed genealogy of the descendants of their ancestors, who settled in Canada in 1874. These are generation I of Figure 1, which is the portion of the genealogy pertinent to the present report.

By selecting cousin matings of descend- ants of 1-2 and 1-8, two Bu (a+) x Bu (a+)

Su ported in part by The National Foundation and gy Grant HD 00527-05 from the National Insti- tutes of Health, U.S. Public Health Service.

Received for publication October 13, 1966; ac- cepted November 8, 1966.

matings with 20 children were found (IV 53 x 358 and IV 345 x 396 of Figure 1). All those who were Bu (a+) were tested for strength of reaction (dosage) with the orig- inal anti-Bua serum, Char; Soch does not indicate dosage. The results are shown in the figure. In each of the two families the Bu (a+) parents had single dose reactions; of the 20 children three had double dose reactions, 11 had single dose reactions, and six were negative. The double dose reac- tion was interpreted as an indication of a BuaBua individual who should, by hypoth- esis, be Sm-negative. Two adults of genera- tion V, Erw and Leo, had this reaction. Their erythrocytes were used to absorb the anti-Sm serum which, in its native state, contains a powerful anti-D. The absorbing cells removed the anti-D and left the anti8m unchanged. The Sm data in Fig- ure 1 were then obtained.

All the information in the figure, as well as previously published information,4 is compatible with the assumption that Bua and Sm are products of allelic genes. If the Sm+ parents of the family reported by Schmidt et aZ.5 were Bu(a+), as is highly probable, then adding their six children to the 21 of the three Bu(a+)Sm+ x Bu(a+)Sm+ matings in the figure gives a phenotypic distribution of seven Bu (a+) - Sm-, 12 Bu(a+)Sm+, eight Bu(a-)- Sm+. Furthermore, the two Bu (a+)Sm- x Bu(a-)Sm+ matings, Erw and Leo and their wives, have produced only Bu (a+)- Sm+ children (five). Data on other mat- ings defined by the two sera are too few to mention. Our present deductions from the serologic evidence are that the pheno- type Bu (a+) Sm- probably represents the Bun homozygote, the phenotype Bu (a+)-

92

Vdume 7 Number 2

ON THE BLOOD GROUP ANTIGENS Bua AND Sm 93

I

II

111

IV

V

DOUBLE DOSE nu (a+ ) DEDUCED BU’ DUO + + + + + + VI @ SINGLE DOSE Bu ( a + ) DEDUCED Bua h

DEDUCED Sm Sm a @ BU (a - )

+ h -POSITIVE

- Sm - NEGATIVE

0 DEAD

FIG. 1. The fragment of the Mennonite kindred in which the Bu(a+) x Bu(a+) matings occurred. The identifying numbers of generations 11, 111 and IV are the kindred numben of known descendants of I-1x2 and 13x4. Generations V and VI (as yet incomplete) have not been given kindred numbers.

Sm+ the heterozygote, and the phenotype Bu (a-)Sm+ the Sm homozygote. Dr. Car- ter Denniston, Department of Human Genetics, University of Wisconsin, kindly considered our data as a statistical problem in linkage. Without giving his calculations, we quote his general conclusion: “While one can’t prove allelism, the data reject any recombination fraction greater than 10 per cent.”

Diego and Auberger, separate system status may be claimed. (Miss Giles tested many of the people in the figure with anti-Ytb; all were negative.) In the meantime we think it wiser not to add a new terminology that might have to be changed shortly.

Acknowledgments

We are deeply indebted to Dr. Halina Seyfried for the anti-Bua, to Miss Pauline Schmidt for the

The inheritance of Bua has been reported anti-Sm, to Mn. Jane Swanson for anti-Doa, to Miss to be independent of nine blood group Carolyn Giles for typing with anti-Csa and anti-Ytb

and for confirming Leo’s Sm typing, and to Dr. systems and of sex*1’ We have now found Carter Denniston for his statistical analysis. Miss it to be independent of the antigen Doa Schmidt also kindly confirmed the Sm typing of described by Swanson et al.,7 and Miss Erw and Leo using a second example (Herren) Carolyn Giles has found it to be inde- Of anti-sm*

We are indebted more than we can say to the pendent Of an which she and many members of the kindred who so generously her associates reported.2 If the inheritance cooperated with us, to their family physicians and can be shown to be independent of Yt, to laboratory personnel of the community hospitals.

94 LEWIS, ET AL. Transfusion Mar.-Apr. 1967

References 1. Anderson, C., J. Hunter, A. Zipursky, M. Lewis,

and B. Chown: An antibody defining a new blood group antigen, Bua. Transfusion 3: 30, 1963.

2. Giles, C. M., M. C. Huth, T. E. Wilson, H. B. M. Lewis, and G. E. B. Grove: Three examples of a new antibody, anti-Csa, which reacts with 98% of red cell samples. Vox Sang. 10:405, 1965.

3. Lewis, M., B. Chown, H. Kaita, and S. Philipps: Further observations on the blood group antigen Bur. Am. J. Hum. Genet. 16256, 1964.

4. Lewis, M., B. Chown, R. P. Schmidt, and J. J. Griffitts: A possible relationship between the blood group antigens Sm and Bua. Am. J. Hum. Genet. 16:254, 1964.

5. Schmidt, R. P., J. J. Griffitts, and F. F. North-

man: A new antibody, anti-Sm, reacting with a high incidence antigen. Transfusion 2: 338, 1962.

6. Seyfried, H., K. Frankowska, and C. Giles: Further examples of anti-Bna found in im- munized donors. Vox Sang. 11:512, 1966.

7. Swanson, J., H. F. Polesky, P. Tippett, and R. Sanger: A “new” blood group antigen, Doa. Nature 206:313, 1965.

Marion Lewis, B.A., Research Associate in De- partment of Pediatrics, University of Manitoba, and Rh Laboratory, 735 Notre Dame Ave., Winni- peg, Canada.

Bruce Chown, M.D., D.Sc., Professor of Pediatrics, University of Manitoba, and Rh Laboratory, 735 Notre Dame Ave., Winnipeg, Canada.

Hiroko Kaita, Senior Technologist, Rh Labora- tory, Winnipeg, Manitoba, Canada.