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S Leskowitz

Publications and source records attributed to S Leskowitz.

At least 73 records · Page 4Linked to original sources
PubMed1967

Mechanism of delayed reactions.

Arsanilic acid conjugates of polymers of L-typrosine, glutamic acid, and alanine are immunogenic and can elicit hapten-specific, delayed-hypersensitivity reactions in sensitized guinea pigs. Conjugates of the D-amino acid polymers are neither immunogenic nor capable of eliciting delayed reactions. Mixtures of small amounts of conjugates capable of eliciting a delayed reaction with larger amounts of D-amino acid polymer conjugates produce only small delayed reactions. I suggest that the delayed reaction is an active response requiring the continued participation of immunogenic material in sensitized animals; it is not the reaction of preformed antibody-like material with the antigenic determinant.

Alanine↗
PubMed1967

Tolerance.

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Animals↗
PubMed1966

Immunochemical study of antigenic specificity in delayed hypersensitivity. V. Immunization with monovalent low molecular weight conjugates.

Hapten-specific delayed hypersensitivity was produced by immunization of guinea pigs with arsanilic acid conjugated to N-acetyltyrosine or other small aromatic molecules. Such hapten-specific delayed sensitivity could be passively transferred by peritoneal exudate cells. While a conjugate made from a polymer of D-amino acids was ineffective in producing sensitization, the conjugate made with D-tyrosine was effective, suggesting that the inability of D-amino acid polymers to be broken down by enzymes might be bypassed by use of the monomer. The effectiveness of such monomers in producing delayed sensitivity, but not antibody production, is consistent with a hypothesis that different types of antigenic determinants are involved in the production of each.

Amino Acids↗
PubMed1965

Immunochemical study of antigenic specificity in delayed hypersensitivity. IV. The production of unresponsiveness to delayed hypersensitivity with a single antigenic determinant.

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.

Animals↗