Identification of HTLV-1-specific CTL directed against synthetic and naturally processed peptides in HLA-B*3501 transgenic mice

Chrstian Schönbach, Kiyoshi Nokihara, Charles R.M. Bangham, Ai Kariyone, Sachiko Karaki, Hisatoshi Shida, Kiyoshi Takatsu, Kohji Egawa, Karl Heinz Wiesmüller, Masafumi Takiguchi

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Abstract

Previous studies of CTL responses to influenza peptides in HLA single transgenic mice resulted in the identification of at most one immunodominant epitope. Since HLA-B*3501 is known to present multiple HIV-1-specific T cell epitopes we tested the cellular immune response of HLA-B*3501 transgenic mice to synthetic HTLV-1 peptides mixed with the lipohexapeptide N-palmitoyl-S-[2,3- bis(palmitoyloxy)propyl]cysteinyl-seryl-lysyl-lysyl-lysyl- lysine, which is a biocompatible, T(h)-epitope-independent adjuvant. Eleven of 37 tested HLA-B*3501 binding peptides mounted a CTL response after three in vitro stimulations. The HLA-B*3501 affinity of peptides correlated with their ability to induce CTL in HLA-B*3501 transgenic mice. Seven peptides derived from env-gp46 (VPSPSSTPLL, VPSSSSTPL, YPSLALAPH, and YPSLALAPA), pol (QAFPQCTIL), gag-p19 (YPGRVNEIL), and tax (GAFLTNVPY) proteins induced peptide-specific CTL. Bulk CTL generated by four peptides derived from env-gp46 (SPPSTPLLY, VPSPSSTPLLY, and VPSPSSTPLL) and pol (QAFPQCTILQY) killed peptide-pulsed and recombinant vaccinia-infected target cells. The latter peptides therefore present T-cell epitopes and are vaccine candidates for our transgenic mouse model.

Original languageEnglish
Pages (from-to)102-112
Number of pages11
JournalVirology
Volume226
Issue number1
DOIs
Publication statusPublished - Dec 1 1996

ASJC Scopus subject areas

  • Virology

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    Schönbach, C., Nokihara, K., Bangham, C. R. M., Kariyone, A., Karaki, S., Shida, H., Takatsu, K., Egawa, K., Wiesmüller, K. H., & Takiguchi, M. (1996). Identification of HTLV-1-specific CTL directed against synthetic and naturally processed peptides in HLA-B*3501 transgenic mice. Virology, 226(1), 102-112. https://doi.org/10.1006/viro.1996.0632