MATERNAL IMMUNIZATION MODULATES THE PRIMARY IMMUNE-RESPONSE TO 2-PHENYL-OXAZOLONE IN BALB C MICE/

The development of the antibody repertoire in newborn mice is greatly influenced by idiotypic network interactions. It has been demonstrated that anti-idiotypic antibodies either directly injected or transferre d from the mother may alter the repertoire for life. For an elucidatio n of the underlying mechanisms we have analyzed the primary immune res ponse to 2-phenyl-5-oxazolone (phOx) coupled to chicken serum albumin (CSA) in BALB/c mice after complete disappearance of maternal antibodi es which originated from different stages of affinity maturation. Depe nding on the serum titers of the mothers after primary (1 degrees mo), secondary (2 degrees mo) or tertiary (3 degrees mo) immunization, mat ernal anti-phOx IgG persisted in F1 mice for up to 9 months. In additi on, F1 mice born to 2 degrees mo developed - even without immunization - an anti-phOx IgM titer which reached levels similar to an antigen-i nduced primary response. An enhancement of the early primary anti-phOx as well as anti-CSA response was seen in FI mice born from 1 degrees mo, whereas the response was delayed when born to 2 degrees mo and 3 d egrees mo. The antibody titers in the latter group of mice remained at a lower level for 3 months. In contrast, mice of the F2 generation wh ich received a smaller amount of the same collection of maternal antib odies as F1 mice from 3 degrees mo exhibited a quite different primary response: (i) They showed an earlier onset in their anti-CSA response . (ii) Whereas normally a plateau in antibody titer was reached by the 4th weak after immunization, in 55 % of the F2 mice a prolonged incre ase of the anti-phOx and anti-CSA antibody titers was observed. At 12 weeks after antigenic challenge, titers reached plateau levels of 6 x 10(5) which were never before seen in a primary phOx or CSA response. Thus, depending on its own immunological experience, the maternal immu ne system induces a state of memory in the offspring which results in a faster and/or enhanced immune response in the F1 and F3 generations.