Conditions which favor the C1-fixation by mouse IgG1.

The capacity of mouse IgG1 to mediate activation of the classical complement pathway was reinvestigated with purified C1 and under various conditions. Monoclonal and polyclonal IgG1 antibodies to TNP, which failed to show a haemolytic activity on TNP-SRBC with low epitopic density at physiologic salt concentration, invariably restored their activity when reacted to TNP-SRBC with relatively higher epitopic density and at a reduced salt concentration. Unliganded, monomeric IgG1 too proved to possess an inherent C1-binding capacity, but the susceptibility to competing salt was extremely high. These results were seemingly in accordance with the reduced number of basic amino acids in the plausible C1-binding region of the molecule.