UBC Theses and Dissertations
Characterization of idiotype interactions during the immune response to ferredoxin. idiotype and epitope specific interactions determine the outcome of challenge with antigen Weaver, Michael Stanley
Anti-idiotype antisera were raised in rabbits to two monoclonal antibodies, Fd-1 and Fd-2, with specificity for each of the two antigenic epitopes found on the ferredoxin (Fd) molecule. The anti-idiotype antisera (anti-Fd-1 and anti-Fd-2) were used to demonstrate that one of the idiotypes (Fd-1) was expressed at significant levels in most anti-Fd antisera raised in BIO.BR mice while the second idiotype (Fd-2) was infrequently expressed. Examination of anti-Fd sera raised in other mouse strains demonstrated that expression of the Fd-1 idiotype mapped to the IgH gene complex and was found in the antisera of all mouse strains examined with the Ig-1[sup=b] allotype. When splenocytes from Fd-immune B10.BR mice were treated with anti-Fd-1 and transferred to irradiated syngeneic recipients, the adoptive secondary response was significantly higher in animals receiving treated cells as opposed to control animals which received normal rabbit serum treated cells. This response produced a net increase in antibody to both epitopes and the relative amount of Fd-1 idiotope was not significantly altered. Further studies with separated cell populations showed that the overall increase of anti-Fd antibody produced was attributable to the effects of the anti-idiotypic serum on a population(s) of T cells. Treatment of mice with the Fd-1 monoclonal antibody (which should react with anti-idiotypic cells) had an analogous effect to that of the anti-idiotype. Treated mice produced heightened levels of antibodies directed to both epitopes of Fd. Treatment of mice with second anti-idiotype, anti-Fd-2, was found to enhance the anti-Fd response of B10.BR mice and abrogate the non-responder status of DBA/2 mice. Additional evidence indicates that the Fd-2 idiotype could be expressed on a suppressor cell population which may be a predominant regulatory element in both BIO.BR and DBA/2 mice.
Item Citations and Data