Isogeneic monoclonal antibodies against anti‐α(1 → 3)dextran idiotypes II. Neonatally induced idiotope‐specific suppression: a comparative analysis

摘要

AbstractFrom a panel of isogeneic monoclonal anti‐idiotope antibodies several were used as agents in neonatal idiotope suppression. They differed from one another in isotype, and in idiotope specificity, as described in the preceding report (Eur. J. Immunol.1987.17:255). In their effects they were compared with respect to the following variables: (a) minimum dose required for suppression; (b) duration of suppression, and its relationship to the dose applied neonatally; (c) half‐life of anti‐idiotope in the immune system of the young mice; (d) specificity of suppression as achieved by a given anti‐idiotope: in how far does it affect idiotopes defined by alternate anti‐idiotopes? The following results were obtained: (a) the minimum effective dose varied widely between anti‐idiotopes. One, belonging to the IgM class, was completely ineffective; others varied from ≈ 10 μg/mouse, required for complete suppression, to ≈ 100 μg/mouse. (b) The dose‐response characteristic was independent of whether the state of suppression was tested (by immunization against α(1 → 3)dextran) 26 days or 70 days after neonatal anti‐idiotope treatment. We take this as an indication that the anti‐idiotope effect occurs during an early postnatal period. (c) There appeared to be a relationship between the rate of decay of anti‐idiotope in the system and the dose required for complete suppression: the faster the decay, the more is needed initially. The persistence of effective molecules in the animals appears to depend on their isotype (as has been noted by others before): IgM decays fastest, and was ineffective in our experiments; IgG1stays longest, and the smallest dose was required for suppression. IgG2bwas intermediate. (d) The specificity of neonatal suppression was clearly correlated with the serological specificity of the anti‐idiotope monoclonal antibodies, as well as with the representation of the corresponding idiotopes in physiological anti‐dextran sera, as described in the preceding report: private anti‐idiotopes suppressed their counterpart idiotopes only, while the public anti‐idiotope suppr