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Quantitative blood typing data on Mr. R. B. (r-Gr-G), his wife (R1r), a daughter (R1r-G), and a niece (r-Gr) strongly suggest that these Rh phenotypes are directly indicative of actual Rh genotypes. If so, the antigenic products of r-G are weak Rh2(rh' or C), normal Rh5 (hr" or e), an expression of Rh12 (rh-G) equal to that produced by R-1,2,-3 (r' or dCe) and half of what is produced by R1 (R or D) genes in either homozygous or heterozygous expression, very weak expression of Rh19 (hr-S), absence of Rh31 (hr-B), and slightly weakened expression of Rh17 (Hr-o or 'not D'). The LW status of r-Gr-G cells was equivalent to that of other Rh:-1 erythrocytes. Thus r-G resembles mutant r' in which only Rh5 is expressed normally. The weak Rh2 produced by r-G reacted much better with one Rh2 antiserum than with another. Rh21 (C-G) had been used to denote such additional reactivity, but one reagent that acted as anti-Rh2 in manual tests behaved like anti-Rh21 in instrumented tests. Therefore, anti-Rh21 may only indicate a more efficiently agglutinating anti-Rh2. Mr. R. B. showed no evidence of congenital stomatocytic hemolytic anemia characteristic of Rh-null or Rh-mod. Finally, anti-Rh12 eluates, recovered either sequentially from r'r followed by R2r or singly from r-Gr-G, agglutinated chimpanzee red cells more efficiently than did either anti-Rh1 (D) or anti-Rh4 (c), a result consistent with expectation for serological crossreactivity between Rh1 and Rh21.
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Rosenfield et al. (1975) studied this question.
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