Injections of various conjugates of arsanilic acid into newborn guinea pigs produced a specific tolerance in respect to subsequent development of hapten-specific delayed hypersensitivity. In general, larger polyvalent conjugates produced longer lasting and more profound suppression of delayed sensitivity than did the smaller ones. Carrier injections alone were ineffective. At lower doses of conjugate, breakthrough of tolerance occurred first with animals immunized with the heterologous carrier conjugate.
The duration of tolerance produced by injection of monovalent conjugates into neonates is in contrast to the transient inhibition produced by the same conjugates in previously sensitized animals, suggesting that different target cells may be involved in these two phenomena.