McGuire D, Rosenfield R E, Wong K Y, Heller C, Rubinstein P, Allen F H, Walker M E, Lewis M
Vox Sang. 1976;30(6):430-40. doi: 10.1111/j.1423-0410.1976.tb02848.x.
Three Rhmod siblings were found to have identical Rh: w1, w2, -3, -4, w5 (see article) phenotypes. All had stomatocytic hemolytic anemia. On quantitative hemagglutination studies, as well as on hand tests, all Rh antigens were not equally depressed. Rh17 (Hr0, 'not D') and Rh29 (RH, 'total Rh') were both normal. Rh5 (hr", e) was only slightly depressed. Rh25 (LW) had 50% of the expression expected in normal Rh:-1 cells. Rh1 (Rh0, D), Rh13 (RhA), Rh14 (RhB), Rh15 (RhC), and Rh16 (RhD), were severely depressed. Rh2 (rh', C) was depressed, while Rh7 (rhi, Ce) was absent. Both Rh19 (hrS) and Rh31 (hrB) were depressed. Rh12 (rhG, G) was distinctly depressed, scoring considerably less than rGrG red cells. The unrelated parents, the child of the proposita, and some siblings of each parent showed lessened depression of Rh antigens without displaying the consistent pattern that might be expected from a presumed single suppressor gene. Absence of a consistent pattern may have resulted from differing Rh genotypes, but a frequently observed depression involved Rh14, Rh15, and Rh16 (RhB, RhC, and RhD) without an effect on either Rh1 (RH3 or D) or Rh13 (RhA).