Allergic encephalomyelitis in monkeys induced by a peptide from the A1 protein.

A major disease-inducing site for induction of experimental allergic encephalomyelitis in monkeys exists in Peptide P 14, the 37-residue segment of the A1 protein comprising its COOH-terminus. The peptide appears to contain the dominant encephalitogenic determinant, since it was as active as the A1 protein on a molar basis. By contrast, the 9-residue tryptophan region and the Peptide R region, active in guinea pigs and rabbits, respectively, were comparatively inactive in monkeys. The clinical and histologic expression of the disease produced by Peptide P 14 appeared identical to that induced by the intact A1 protein.