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• W1500900725 startingPage "307" @default.
• W1500900725 abstract "Many T cell responses are dominated by restricted TCR expression and can range from repeated usage of particular TCR Vbeta- and/or Valpha-elements, to the preferential usage of both V- and J-elements, often in conjunction with conserved V-D-J or V-J junctional sequences. Cytotoxic T lymphocytes specific for a Kb-restricted determinant from the herpes simplex virus glycoprotein B (gB) preferentially express a dominant TCRBV10 beta-chain with sequence conservation of a tryptophan-glycine located in the V-D junction. Here we have examined whether immunisation of C57BL/6 mice with the gB-peptide can mimic the CTL response seen after HSV-1 infection. Immunisation with the gB-peptide resulted in the generation of gB-specific CTL that showed a similar TCRBV10 bias to that observed after HSV-1 infection. When the gB-determinant was expressed as a part of a fusion protein, immunised mice again exhibited the TCRBV10 bias with the junctional sequence conservation in the responding CTL. C57BL/6 mice were then immunised with variants of the gB-peptide that contained amino acid substitutions at positions previously predicted to contact the TCR beta-chain CDR3. Analysis of the TCRBV usage of variant specific CTL lines showed that substitutions at the TCR-contact positions 4, 6 and 7 of the gB-peptide resulted in a loss of the TCRBV10 bias. These results suggest that the TCRBV10 bias seen in gB-specific CTL after HSV-1 infection is due to antigenic selection by the minimal peptide and is determined by residues proposed to contact the TCR beta-chain CDR3." @default.
• W1500900725 created "2016-06-24" @default.
• W1500900725 creator A5003005203 @default.
• W1500900725 creator A5066955897 @default.
• W1500900725 date "1998-04-01" @default.
• W1500900725 modified "2023-09-26" @default.
• W1500900725 title "A dominant V β bias in the CTL response after HSV-1 infection is determined by peptide residues predicted to also interact with the TCR β -chain CDR3 fn2 fn2Thiswork was supported by the Australian Research Council, the Australian National Health and Medical Research Council and an Australian Research Council Senior Research Fellowship (to FRC)." @default.
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• W1500900725 doi "https://doi.org/10.1016/s0161-5890(98)00051-0" @default.
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• W1500900725 hasPublicationYear "1998" @default.
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