Abstract
Sensitization of sheep E with nurse shark (N) serum resulted in the formation of EAN if the serum was heat-inactivated or reacted in 0.04 M EDTA at 30°C, of EANC′1N if the serum was freeze-inactivated or reacted in 0.04 M EDTA at 0°C. Guinea pig (g.p.) complement or sup. I readily lysed EANC′1N but not EAN due to a complete C′1 incompatibility, which could also be demonstrated in vivo: in the absence of C′1N, the then non-complement-fixing antibody was not only tolerated by guinea pigs, but it protected them against lethal Forssman shock. Shark C′1 lysed EARa and its intermediate complexes with g.p.-C′ only to the extent of its contamination with antibody; a noteworthy exception was the complex EARaC′1–C′8 g.p. A large variety of Forssman positive and negative erythrocytes were agglutinated and sensitized by the shark's natural antibodies. Young animals had much less antibody but a fully reactive complement system. A powerful, nontoxic inactivator of mammalian C′4 could be isolated and separated from antibody, C′1, and most other serum proteins by gel filtration of low ionic strength precipitates from normal shark serum.