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From La Rabida University of Chicago Institute and Departments of Pathology and Biochemistry, East 65th Street at Lake Michigan, Chicago, Illinois 60649
Abstract
We have examined the ability of anti-receptor antibody (ARA) to induce specific unresponsiveness to the hapten, phosphorylcholine (PC), in neonatal and adult mice. When ARA is given to adult mice, suppression is of short duration. Cells from such mice are responsive in vitro, indicating that suppression in vivo is probably due to blockade of receptors by persisting ARA. ARA given to neonatal mice induces long-term unresponsiveness. These mice apparently have decreased numbers of PC-responsive cells, since cells from such mice are unresponsive both in vitro and in adoptive transfer. Furthermore, cells from neonatally suppressed animals do not suppress the response of normal cells either in vitro or in adoptive transfer, indicating that unresponsiveness is most likely not due to active suppression. We therefore conclude that ARA given to neonates depletes the clone of receptor-bearing cells at the time ARA is given. Clonal depletion may result from antibody-dependent cell mediated cytotoxicity.
Footnotes
1 This research is dedicated to the Max Goldenberg Foundation for its generous help.
2 This work was supported by United States Public Health Service Grants AI-11080, AI-09268, and AI-10242.
3 MSTP Trainees supported by United States Public Health Service Grant 2T05GMO 1939-06.
4 Recipient United States Public Health Service Career Development Award AI-70559.
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