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Modification of T cell antinuclease idiotype expression by in vivo administration of anti-idiotype

Immunization of BALB/c mice with nuclease leads to the production of anti-nuclease antibodies bearing a set of cross-reactive idiotypes (Id) distinct from those produced by B10.D2 mice after similar immunization. In both strains, such immunization with nuclease also leads to the production of spleni...

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Detalles Bibliográficos
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1982
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186558/
https://www.ncbi.nlm.nih.gov/pubmed/6172540
Descripción
Sumario:Immunization of BALB/c mice with nuclease leads to the production of anti-nuclease antibodies bearing a set of cross-reactive idiotypes (Id) distinct from those produced by B10.D2 mice after similar immunization. In both strains, such immunization with nuclease also leads to the production of splenic T helper cells (TH), which provide nuclease- specific help in an in vitro plaque-forming cell response to nuclease- TNP. Pig anti-(BALB/c antinuclease) anti-idiotypic antibodies (pig anti- BALB/c Id) react only with TH of nuclease-primed BALB/c and not with B10.D2 animals. After administration of pig anti-BALB/c Id in complete Freund's adjuvant to BALB/c and B10.D2 mice, Id-bearing nonantigen- binding molecules were induced in both strains. Such treatment also resulted in the induction of nuclease-specific splenic TH cells in both strains. BALB/c TH cells induced by anti-Id, like the majority of nuclease-primed BALB/c TH cells, bore BALB/c Id, as shown by their functional elimination with anti-Id plus complement. B10.D2 TH cells induced by anti-Id, unlike TH cells from nuclease-primed B10.D2 mice, also bore BALB/c idiotypic determinants by the same criterion. Thus, it appears that one can manipulate the expression of Id on serum immunoglobulins and on antigen-specific TH cells by administration of exogenous anti-Id reagents. These results have implications both for network interactions in the immune response and for the genetic basis of Igh-C linked Id expression.