The subtype AxB has been encountered and described, along with two new examples of the subtype Ax. Anti-A and anti-A,B that has been absorbed by and eluted from erythrocytes of subtype Ax are sensitive to at least partial inhibition by the salivary secretions of the Ax person, thereby implying that A determinants are expressed in the salivary secretions as well as on the erythrocytes. Saliva of the AxB person did not possess such inhibitory activity. However, family study disclosed that this person was likely to possess an unusual A2B genotype in which the B gene suppresses, at the phenotypic level, the expression of paired A. Furthermore, an underlying disease, myeloid metaplasia, may have further suppressed the expression of A determinants on both erythrocytes and in salivary secretions. Three other pedigrees revealed suppression of A by paired B, and in one instance, the genotype A1B was found to give rise to the phenotype A2B. Some population studies fail to demonstrate satisfactory Hardy-Weinberg equilibrium when tested in accordance with the usual four allele theory of inheritance for the A1A2BO phenotypes. An additional allele, suppressor B (B[unknown]) was assumed for five such studies, and a more satisfactory fit between expected and observed values was obtained.

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