Abstract
Heat-labile opsonins to pneumococci in normal mammalian sera, unlike antibodies, fail to interact with the bacteria at 0°C and require Ca++ and/or Mg++. They are readily removed from serum by antigen-antibody complexes that fix complement (C) and are inhibited by reagents that inactivate various C components. The principal heat-labile opsonin to pneumococci is activated C3 (C3b), but a slight enhancing effect is exerted by one or more of the late-reacting components of the hemolytic complement system (C5-C9). Since heat-labile opsonins are immunologically polyspecific, they presumably play a broad protective role in the early (preantibody) phase of acute bacterial infections.
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Selected References
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