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Antibodies directed against the common acute lymphoid leukemia antigen (CALLA) were obtained from 2 hybridomas: J5 (Schlossman, mice sensitized with patient ALL cells), and Vil-A1 (Knapp, sensitization with the Reh cell line). The percentage of lymphoid cells reacting with these 2 monoclonal antibodies were compared. Antibody dilution curves indicated that the dilutions used yielded maximum percentages of positive cells. The percentage of CALLA-positive cells with the J5 antibody was significantly (p less than 0.001) higher than that found with the Vil-A1 antibody in 16 non-neoplastic inflammatory tonsils and in 13 non-Hodgkin lymphoma and chronic lymphatic leukemia lymph-nodes (p less than 0.05). In contrast, the difference between CALLA positive cells with J5 and Vil-A1 was not significant (p greater than 0.5) in 19 acute lymphoid leukemias. The difference between the ALL-cells, presumably pre-B, and the B-cells from the non-ALL subjects was also statistically significant (p less than 0.01). The results suggest that the two hybridomas form antibodies against different CALLA epitopes. Vil-A1 seems somewhat more specific for ALL than J5.

The reaction was studied of the J5-monoclonal antibody with the common acute leukemia antigen (CALLA) on non-malignant human tonsil lymphatic cells, which were double labelled also with antibodies against the B1 and HLA-DR antigens or the kappa and lambda light chains. There were few cells (mean 0-1.4%) which were positive with J5 but not B1. Other percentages of labelled cells depended on the order in which the antibodies were added. If the J5-antibody was added first, more B1 positive cells are found than if the B1 antibody is added first. Similarly, a significant (p less than 0.01-p less than 0.001) increase (3.3-18.8%) in the percentage of cells positive with J5 was found when the B1, kappa, and HLA-DR antibodies were added first, but not if antibody against lambda chains is added first. This difference was most pronounced and most significant for B1. This difference can be explained inter alia by steric differences between antibody conjugated and non-conjugated antigens followed by unmasking of other antigens. Double labelling is thus not equal to two single labellings.