Author(s): Masaki H, Yamane S, Irimajiri K, Horiuchi A, Yamaguchi J,
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Abstract We have previously reported a CD3+ CD4+ CD8- T cell line, J-2R which specifically recognized J558 individual idiotope (IdI) of anti-alpha (1-->3) dextran antibodies in an I-E(d) restricted manner. The J-2R proliferated in response to J558 IdI-derived peptides; however, the ability of the peptides to evoke the proliferation of J-2R was different. In the present study, we investigated the interaction between J558 IdI-derived peptides and I-E(d) molecules in competition experiments using a M104E IdI-derived peptide, M88-105. The M88-105 inhibited the proliferation of J-2R induced by J558 IdI-derived peptides. Furthermore, the proliferation induced by the peptides J92-109 and J96-105 was inhibited by the M88-105 at much lower inhibitor/antigenic peptide ratios, compared to the proliferation induced by the J88-105. Thus, shift of the framework to C-terminus and deletion of N-terminus amino acid residues from the 18-mer peptide J88-105 made the peptides more susceptible to the inhibition by the M88-105. Sequencing of the J-2R T cell receptor (TcR) revealed that J-2R used TcR, V alpha 1, J alpha 44; V beta 15, D beta 1, J beta 1.5. These results suggest that the peptides, J88-105, J92-109 and J96-105, directly bind to I-E(d) molecules, and that the capacity of J558 IdI-derived peptides to activate J-2R depends on the affinity to the I-E(d) molecules.
This article was published in J Clin Lab Immunol
and referenced in Journal of Bioterrorism & Biodefense