Thus the mechanisms of the defects of DAF and/or CD59 in human leukaemia cell lines are not uniform, and in most cases are different from that proposed to cause PNH.
While in normal individuals all these molecules are broadly expressed on leukocytes, in patients with leukemias the following deviations were observed: (a) at least one of the examined molecules was missing in 64/68 cases (94%); in 12/68 cases (18%) both molecules LFA-1 and ICAM-1 were missing, in 37/68 (54%) either LFA-1 or ICAM-1, and in 15/68 cases (22%) adhesion molecules other than LFA-1 or ICAM-1 were missing; (b) the expression of CD11a/CE18, CD58, CD59 on leukemic cells was heterogeneous, without any clear correlation to the subclass of leukemia; (c) in the majority of cases, CD54 (45/68; 66%) and CD44 (36/68; 53%) were missing, however showing a tendency of expression on leukemic cells with more mature immunophenotype.