Abstract
The D antigen of the Rhesus blood group, an erythroid-specific cell surface marker, is expressed by all morphologically recognizable human nucleated red blood cell precursors including, in low density, the pronormoblast. The object of the present study was to determine the expression of the D antigen by committed erythroid progenitors. Under conditions that produced complete inhibition of BFU-E and CFU-E by known cytotoxic antisera, no significant inhibition was produced by anti-D. Use of anti-human IgG (rabbit) to increase sensitivity and trypsinization to reveal cryptic Rh determinants were both without inhibitory effect. Erythroid bursts and colonies grew normally in methylcellulose that contained anti-D. The addition of anti-D to day 7 BFU-E did not inhibit their proliferation to mature bursts at day 14. These results suggest that the D antigen is not expressed by human committed erythroid progenitor cells. The D antigen is therefore an erythroid-specific differentiation marker, rather than an erythroid- lineage-specific antigen. The development of expression of the D antigen during erythropoiesis parallels that of band 3 protein, to which anti-D has been reported to bind. Lack of Rh expression by committed erythroid progenitors is consistent with the rarity of red cell aplasia in Rhesus hemolytic disease of the newborn and in idiopathic and drug-induced autoimmune hemolytic anemia in which the autoantibodies have apparent Rh specificity. These results imply that Rh compatibility is not a contraindication to human bone marrow transplantation.
Missense
RHD
single nucleotide variants induce weakened D antigen expression by altering splicing and/or protein expression
