Production of auto-anti-idiotypic antibody during the normal immune response to TNP-ficoll. I. Occurrence in AKR/J and BALB/c mice of hapten-augmentable, anti-TNP plaque-forming cells and their accelerated appearance in recipients of immune spleen cells.
Attempts were made to elucidate the cause of the downward regulation of the splenic plaque-forming cell (PFC) response in AKR/J and BALB/c mice between days 4 and 7 after a single intravenous injection of 2,4,6,trinitrophenyl- lys-Ficoll(TNP-F). AKR/J spleen cells, taken 7 d after injection of TNP-F, were transferred, together with TNP-F, into normal AKR/J mice. The day-3 or - 4 PFC response of the recipients was much lower than that of recipients of normal cells. However, the suppression was only apparent because the presence of 10(-8)-10(-7) M 2,4,6-trinitrophenyl-epsilon-amino-n-caproic acid (TNP- EACA) (or 10(-7)-10(-6) M 2,4,-dinitrophenyl-epsilon-amino-n-caproic acid) in the PFC assay caused a dramatic increase in observed PFC, averaging 298 percent on day 3 and 122 percent on day 4. Recipients of normal cells showed no such hapten-augmentable PFC. T-depleted immune spleen cells did not cause any apparent suppression of the response to TNP-F, but hapten-augmentable PFC in recipient spleens were again prevalent. Suppression of the PFC response, as well as hapten-augmentable PFC, were seen after transfer of immune serum. It was postulated that hapten augmentation of PFC was caused by displacement of auto-anti-idiotypic antibody from the surface of blocked antibody- synthesizing cells. Further studies showed that such hapten-augmentable PFC occurred in the spleens of a large percentage of both AKR/J and BALB/c mice examined after day 4 of the primary response to TNP-F. Thus, it was hypothesized that the downward regulation of the magnitude and, possibly, also of the heterogeneity of the splenic-PFC response was due to an auto-antibody response to one or more major idiotypes of the anti-TNP response.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis*; D001323:Autoantibodies / Q000032:analysis*; D005362:Ficoll / Q000031:analogs & derivatives / Q000276:immunology*; D006241:Haptens / Q000276:immunology*; D007130:Immunoglobulin Idiotypes; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C / Q000276:immunology; D008815:Mice, Inbred Strains / Q000276:immunology*; D011134:Polysaccharides / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology*; D014301:Trinitrobenzenes / Q000276:immunology
D000888:Antibodies, Anti-Idiotypic; D001323:Autoantibodies; D006241:Haptens; D007130:Immunoglobulin Idiotypes; D011134:Polysaccharides; C020529:TNP-ficoll; D014301:Trinitrobenzenes; D005362:Ficoll