Ir gene defects may reflect a regulatory imbalance. I. Helper T cell activity revealed in a strain whose lack of response is controlled by suppression.
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."
D000818:Animals; D001717:Birds; D002645:Chickens; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D005802:Genes, MHC Class II; D007165:Immunosuppression Therapy; D007700:Kinetics; D008198:Lymph Nodes / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D009113:Muramidase / Q000276:immunology; D010527:Perissodactyla; D010641:Phenotype; D013601:T-Lymphocytes / Q000276:immunology*
D009113:Muramidase