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Ferredoxin T cell idiotype : linkage to immunoglobulin heavy chain alleles or the major histocompatibility complex

University of British Columbia

An anti-idiotypic antiserum was raised in rabbits to a monoclonal antibody with specificity for one of the two antigenic determinants on the ferredoxin (Fd) molecule. The monoclonal antibody (Fd-B2) was derived from fusion of spleen cells from Fd-immune B10.BR (H-2[sup k], Igh[sup b]). Examination of an extensive number of samples of Fd-immune serum from B10.BR and other mouse strains established that the Fd-B2 idiotype is essentially never present in such sera in detectable concentrations (> 30 ng/ml). Administration of the anti-idiotypic antibody (anti-Fd-B2) i.v. to B10.BR mice, or treatment of B10.BR T-cell enriched populations with anti-Fd-B2 + complement prior to adoptive transfer to irradiated BI10.BR recipients followed by challenge with Fd resulted in a significant increase in the production of anti-Fd antibodies. This effect was specific and was not accompanied by a change in expression of the Fd-B2 idiotype in the antibody produced. Similarly, injection of 10 μg of Fd-B2 into B10.BR mice resulted in an enhanced anti-Fd response. When similar experiments were carried out using B10.D2 mice (H-2[sup k], Igh[sup b]), which are genetic non-responders to Fd, it was observed that treatment with anti-Fd-B2 followed by challenge with Fd resulted in production in treated animals of significant levels of antibody to Fd. Again, the antisera thus produced did not contain detectable levels of the Fd-B2 idiotype. Further experiments using high responder (H-2[sup k]) mice with Igh allotypes differing from the BIO strains (C57/BR, Igh[sup a], and RF/J, Igh[sup c]), showed that treatment of these animals with anti-Fd-B2 also resulted in a highly significant enhancement of the anti-Fd response. The implications of these findings are discussed.

Text

2010-04-22

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http://hdl.handle.net/2429/24031

Microbiology and Immunology

University of British Columbia

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