Abstract
Previous data have shown that sera from patients with ALL contain a material which will block the activation of C3 by both the classical and alternative pathways. An in vitro assay was established to test whether or not this “inhibitor” will prevent complement-mediated killing of normal peripheral lymphocytes (L) or bone marrow-derived malignant lymphoblasts (LB). This assay utilizes L or LB as a target cell, antilymphocyte globulin, and serum; cell death is measured by the uptake of 5% eosin. With normal human serum (NHS), the extent of killing of L or LB depends upon the concentrations of target cells, antibody, and serum as well as the time of incubation at 37° C. Using optimal conditions with ALL sera or with NHS to which purified “inhibitor” has been added, the average killing was decreased by 64%. Increasing Ab concentration two fold, serum concentration five fold or the time of incubation three fold did not completely correct the defect with ALL sera. This “inhibitor” is present in NHS and appears to function by modulating the biologic activity of C3. At diagnosis or relapse, patients with ALL may be deregulated in the elaboration of this material. The resultant excess of the “inhibitor” apparently leads to blockade of the effects of antibody and complement in eliminating tumor cells.
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