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Active and Inactive States of Immunologic Unresponsiveness¹

From the Department of Medical Microbiology, School of Medicine, University of California, Davis, California 95616

Abstract

Immunologic tolerance was induced in newborn mice by administration of 1, 5, 10, or 20 mg of lysozyme. These mice were subsequently challenged with a mixture of lysozyme and bovine serum albumin (BSA), or with a covalently coupled conjugate of lysozyme and succinylated BSA. When challenged at 6 weeks of age none of these mice responded to lysozyme when administered admixed with BSA. Of the mice challenged with the lysozyme-SBSA conjugate, those tolerized with 1 or 5 mg of lysozyme responded with antilysozyme antibodies but those tolerized with 10 or 20 mg of lysozyme did not. When challenged at 10 weeks of age, mice which had been tolerized with 20 mg of lysozyme mounted a low level antilysozyme response to both the mixture and the conjugate. Assessment of the response of these animals to BSA and SBSA revealed that the anti-SBSA responses of the conjugate-challenged animals were significantly suppressed whereas the anti-BSA response of the mixture-challenged animals was unaffected.

Tolerance was also induced in adult mice, by the injection of 20, 50, or 100 mg of lysozyme. When challenged 12 days after cessation of the tolerizing regimen, all of these mice exhibited suppressed antilysozyme responses regardless of the challenge antigen, although the antilysozyme responses to the conjugate were slightly higher than to the mixture. No suppression of either anti-BSA or anti-SBSA responsiveness was seen in any of these adult tolerant animals.

It was concluded that administration of low doses of tolerogen to neonatal mice results in only T cell tolerance whereas administration of higher doses of tolerogen also effects B cell responsiveness. Furthermore, neonatally induced tolerance appeared to involve some form of active suppression which did not appear to be a factor in the adult tolerized mice. This suppression was only demonstrable at the B cell level.

Footnotes

¹ This work was supported in part by United States Public Health Service Grant AM-15174 and National Science Foundation Grant GB-30697.

² Conducted during the tenure of Postdoctoral Fellowship 1-FO2-AM-35714 from the National Institutes of Health.