To The Editor.
—Cooperation among immunohematologists and clinical hematologists in identifying relationships between defective membrane hemolytic states and null blood types is urged by Schmidt in the May Archives (139:570-571, 1979). It was this sort of collaboration that in fact led to the elucidation of the hemolytic nature of the McLeod phenotype. This anomaly of the Kell system, named after the propositus, was initially reported in 1961 by Allen et al1 as one of poorly understood weak reactivity to Kell antiserums. It was subsequently discovered that a minority of boys with X-linked chronic granulomatous disease (CGD) exhibited similar weak Kell antigenicity and were prone to isosensitization in this system if they had transfusions. The suspicion that they had the McLeod phenotype later proved to be the case.2 At any rate, from 1961 to 1975, the propositus was the only person without CGD known to have the phenotype.As