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Antibodies directed against the capsular polysaccharides (Ps) of encapsulated pathogenic bacteria can protect the host against infection with such organisms. The immune response to Ps, however, does not develop until relatively late in ontogeny. We have, therefore, studied alternative ways to stimulate anti-Ps antibody responses in neonates, namely priming with idiotype (Id) and anti-Id. We believe that these studies provide the first demonstration of the use of an anti-Id antibody to prime for protection against a bacterial infection and the first demonstration of the ability of a monoclonal anti-Id to prime for protection against any microbial infection. We have used a monoclonal IgM Id, anti-K13 capsular antibody, and a monoclonal IgG1 anti-Id in studies of the effects of administration of anti-Id or Id within 24 h after birth on the ability of mice to respond to subsequent immunization and challenge with live bacteria. These studies show that neonatal administration of 1 micrograms of Id or 50 ng of anti-Id lead to significantly enhanced protection in mice immunized at 4 wk of age and challenged at 5 wk with an intraperitoneal injection of 20-30 LD50 of E. coli 06:K13:H1, as compared with unprimed or antigen (Ps)-primed controls. Mice primed at birth, immunized at 12 wk of age, a time when they can respond fully to Ps itself, and challenged 1 wk later, were still significantly protected by anti-Id priming but no longer showed the effects of Id. We conclude that administration of protective Id early in life may serve a dual function in providing immediate passive protection as well as priming for protective antibodies upon subsequent antigen exposure.

Neonatal administration of idiotype or antiidiotype primes for protection against Escherichia coli K13 infection in mice.