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The Journal of Immunology, 1979, 123: 961-967.
Copyright © 1979 by The American Association of Immunologists, Inc.

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Ir Gene Defects May Reflect a Regulatory Imbalance

I. Helper T Cell Activity Revealed in a Strain Whose Lack of Response Is Controlled by Suppression1

Barbara A. Araneo2, Robert L. Yowell and Eli E. Sercarz

Department of Microbiology, University of California, Los Angeles, Los Angeles, California 90024

Abstract

A singular responsiveness to HEL was revealed in a peripheral lymphoid compartment of the genetically nonresponsive H-2b mouse. Although i.p. injection of HEL induces suppression and a lack of anti-HEL production, following footpad injection there is an early emergence in the popliteal lymph node (P-LN) of HEL-specific helper activity and plaque-forming cells. Furthermore, the early P-LN transiently expresses one of two T cell types needed for initiation of suppression. Delayed recruitment of the second required cell-type permits the induction of efficient suppression. There is only a short period during which there is concurrent representation of the two T cell subpopulations, and by mixing early and late deficient P-LN T cells, suppression could be established. The general implication of these results is that although a vigorous helper cell potential may exist in a strain nonresponsive to a multideterminant antigen, it can be obscured by a regulatory cell imbalance that results in the manifestation of a generalized Ir gene "defect."

Footnotes

1 This work was supported by Grants CA-24442 and AI-11183 from the National Institutes of Health.

2 B. A. was the recipient of a Postdoctoral National Institutes of Health Fellowship.




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