Chemotactic activity in the sera of patients with glomerulonephritis was compared under three simultaneously performed conditions: (1) incubation with buffer at 37 °C (CF-UNACT); (2) incubation with immune complexes at 37 °C (CF-ACT); (3) immediate heating at 56 °C (CF-56 °C). In all cases the generation of chemotactic factors was terminated by standard ‘heat-inactivation’ at 56 °C. Patients’ CF-UNACT was similar to that of controls; patients’ CF-ACT was significantly less than controls’, but patients’ CF-56 °C was significantly greater than controls’. Patients’ CF-ACT and CF-56 °C were largely C5-dependent and were quantitatively similar. These divergent abnormalities could not be explained by spontaneous in vivo or in vitro (i. e., blood clotting) generation of complement chemotactic factors, the absence of Hageman factor-dependent chemotactic activity, or the presence of humoral inhibitors in patients’ sera. It appears that initial 56 °C heating liberates C5-dependent chemotactic activity, a procedure that is usually believed to block its formation. Terminal 56 °C heating after 37 °C incubation did not generate such activity in CF-UNACT. The duration or sequence of heating at 56 °C, or both, are critical determinants for final expression of chemotactic activity in patients’ sera, when viewed in relation to 37 °C incubation
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