Production of auto-anti-idiotypic antibody during the normal immune response: Changes in the auto-anti-idiotypic antibody response and the idiotype repertoire associated with aging Academic Article uri icon

Overview

MeSH Major

  • Aging
  • Antibodies, Anti-Idiotypic
  • Antibody Formation
  • Autoantibodies
  • Immunoglobulin Idiotypes

abstract

  • Hapten-augmentable plaque-forming cells (PFC) are cells whose secretion of antibody is specifically inhibited by surface-bound auto-anti-iodotype antibody that can be displaced by hapten. This study showed that the percentage of hapten-augmentable PFC present in mice during the primary response to trinitrophenylated Ficoll (TNP-F) increases with age. The data suggest that there is a relative increase in the auto-anti-idiotypic antibody response with age and therefore a greater down-regulation of antibody production. The effect of age on idiotype expression was also studied. Hapten-reversible inhibition of plaque formation was used as an assay for anti-inhibition of plaque formation was used as an assay for anti-idiotype antibody and idiotype-bearing antibody-secreting cells. Sera from aged (21- to 22-month-old) C57BL/6 mice immunized with TNP-F significantly inhibited plaque formation, in a hapten-reversible manner, by spleen cells from 81% of TNP-F-immunized aged mice. However, these sera inhibited plaque formation by cells from only 50% of similarly immunized young adult (6- to 8-week-old) mice and 20% of immature (3- to 4-week-old) syngeneic mice. Similarly, sera from TNP-F-immunized young adult or immature mice inhibited formation of plaques by cells from immunized donors of the same age as the mice from whom the serum was obtained, but only rarely inhibited plaque formation by cells from mice of other age groups. The data thus suggest that the repertoire of TNP-specific idiotypes that are produced in response to TNP-F varies with age in syngeneic mice.

publication date

  • December 1980

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC350374

PubMed ID

  • 6969889

Additional Document Info

start page

  • 6788

end page

  • 92

volume

  • 77

number

  • 11 I