Abstract
The influence of T cell specificity was evaluated with regard to its role in the antibody response against the acetylcholine receptor (AChR) and resulting AChR-dependent muscle dysfunction. The reactivity of immune Th cells was restricted to a small region of the AChR α-subunit (amino acid residues 100-116) reported to be highly immunogenic. T cells primed to this peptide were found to demonstrate significant proliferation when challenged in vitro with either the homologous peptide or the intact AChR. Adoptive transfer of the peptide-immune T cells into immunologically naive recipient rats followed by AChR challenge resulted in the production of anti-AChR antibodies very similar to those produced under the regulation of T cells immune to the entire intact AChR with regard to overall clonotypic heterogeneity (measured by IEF) and their ability to interfere with AChR-dependent muscle contraction. Interestingly, when the threonine at position 106 was substituted with a proline, the resulting peptide continued to be equally, if not exceedingly, capable of stimulating T cell-proliferative responses, but was found to be ineffective at stimulating the levels of anti-AChR antibodies necessary for producing neuromuscular dysfunction.
Original language | English (US) |
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Pages (from-to) | 1654-1660 |
Number of pages | 7 |
Journal | Journal of Immunology |
Volume | 144 |
Issue number | 5 |
State | Published - 1990 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology