Identification of tumor rejection antigen peptide recognized by cytotoxic T lymphocytes on murine leukemia RL♂1 and the effect of vaccination

E. Nakayama, A. Uenaka, Toshiro Ono, T. Aji

Research output: Contribution to journalArticle

Abstract

BALB/c radiation-induced leukemia RL♂1 is an immunogenic tumor. We identified the antigen peptides pRL1a and pRL1b which are recognized by RL♂1-specific cytotoxic T lymphocyte (CTL) by acid extraction, HPLC purification, and direct sequencing. pRL1 peptides were shown to be derived from an untranslated region of the normally expressed akt gene. The murine leukemia virus (MuLV) long terminal repeat (LTR) sequence is inserted directly into the exon of c-akt in RL♂1 leukemia and transcription starts from the cap site of the LTR. Translation appeared to start from the ATG codon created in the six nucleotides of unknown origin which had been inserted into the LTR/akt junction. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not pRL1a peptide itself, generated pRL1a-specific CTL in spleen cells from BALB/c mice. Furthermore, in vivo sensitization of BALB/c mice with pRL1a MAP, but not pRL1a peptide itself, showed a marked inhibitory effect on RL♂1 tumor growth. Depletion of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated in vitro CTL generation. Selective depletion of CD4+ T cells from mice by treatment with anti-CD4 monoclonal antibody (mAb) on in vivo sensitization also abrogated in vitro CTL generation.

Original languageEnglish
Pages (from-to)61-70
Number of pages10
JournalGann Monographs on Cancer Research
Volume48
Publication statusPublished - 1999

Fingerprint

Cytotoxic T-Lymphocytes
Neoplasm Antigens
Leukemia
Vaccination
Terminal Repeat Sequences
Peptides
Antigens
Radiation-Induced Leukemia
Untranslated Regions
Murine Leukemia Viruses
Initiator Codon
Carrageenan
Transcription Initiation Site
Exons
Neoplasms
Spleen
Nucleotides
Macrophages
High Pressure Liquid Chromatography
Monoclonal Antibodies

ASJC Scopus subject areas

  • Cancer Research

Cite this

Identification of tumor rejection antigen peptide recognized by cytotoxic T lymphocytes on murine leukemia RL♂1 and the effect of vaccination. / Nakayama, E.; Uenaka, A.; Ono, Toshiro; Aji, T.

In: Gann Monographs on Cancer Research, Vol. 48, 1999, p. 61-70.

Research output: Contribution to journalArticle

@article{35939676e4c747bdaa4493f4fa4c617e,
title = "Identification of tumor rejection antigen peptide recognized by cytotoxic T lymphocytes on murine leukemia RL♂1 and the effect of vaccination",
abstract = "BALB/c radiation-induced leukemia RL♂1 is an immunogenic tumor. We identified the antigen peptides pRL1a and pRL1b which are recognized by RL♂1-specific cytotoxic T lymphocyte (CTL) by acid extraction, HPLC purification, and direct sequencing. pRL1 peptides were shown to be derived from an untranslated region of the normally expressed akt gene. The murine leukemia virus (MuLV) long terminal repeat (LTR) sequence is inserted directly into the exon of c-akt in RL♂1 leukemia and transcription starts from the cap site of the LTR. Translation appeared to start from the ATG codon created in the six nucleotides of unknown origin which had been inserted into the LTR/akt junction. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not pRL1a peptide itself, generated pRL1a-specific CTL in spleen cells from BALB/c mice. Furthermore, in vivo sensitization of BALB/c mice with pRL1a MAP, but not pRL1a peptide itself, showed a marked inhibitory effect on RL♂1 tumor growth. Depletion of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated in vitro CTL generation. Selective depletion of CD4+ T cells from mice by treatment with anti-CD4 monoclonal antibody (mAb) on in vivo sensitization also abrogated in vitro CTL generation.",
author = "E. Nakayama and A. Uenaka and Toshiro Ono and T. Aji",
year = "1999",
language = "English",
volume = "48",
pages = "61--70",
journal = "Gann Monographs on Cancer Research",
issn = "0072-0151",
publisher = "S. Karger AG",

}

TY - JOUR

T1 - Identification of tumor rejection antigen peptide recognized by cytotoxic T lymphocytes on murine leukemia RL♂1 and the effect of vaccination

AU - Nakayama, E.

AU - Uenaka, A.

AU - Ono, Toshiro

AU - Aji, T.

PY - 1999

Y1 - 1999

N2 - BALB/c radiation-induced leukemia RL♂1 is an immunogenic tumor. We identified the antigen peptides pRL1a and pRL1b which are recognized by RL♂1-specific cytotoxic T lymphocyte (CTL) by acid extraction, HPLC purification, and direct sequencing. pRL1 peptides were shown to be derived from an untranslated region of the normally expressed akt gene. The murine leukemia virus (MuLV) long terminal repeat (LTR) sequence is inserted directly into the exon of c-akt in RL♂1 leukemia and transcription starts from the cap site of the LTR. Translation appeared to start from the ATG codon created in the six nucleotides of unknown origin which had been inserted into the LTR/akt junction. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not pRL1a peptide itself, generated pRL1a-specific CTL in spleen cells from BALB/c mice. Furthermore, in vivo sensitization of BALB/c mice with pRL1a MAP, but not pRL1a peptide itself, showed a marked inhibitory effect on RL♂1 tumor growth. Depletion of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated in vitro CTL generation. Selective depletion of CD4+ T cells from mice by treatment with anti-CD4 monoclonal antibody (mAb) on in vivo sensitization also abrogated in vitro CTL generation.

AB - BALB/c radiation-induced leukemia RL♂1 is an immunogenic tumor. We identified the antigen peptides pRL1a and pRL1b which are recognized by RL♂1-specific cytotoxic T lymphocyte (CTL) by acid extraction, HPLC purification, and direct sequencing. pRL1 peptides were shown to be derived from an untranslated region of the normally expressed akt gene. The murine leukemia virus (MuLV) long terminal repeat (LTR) sequence is inserted directly into the exon of c-akt in RL♂1 leukemia and transcription starts from the cap site of the LTR. Translation appeared to start from the ATG codon created in the six nucleotides of unknown origin which had been inserted into the LTR/akt junction. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not pRL1a peptide itself, generated pRL1a-specific CTL in spleen cells from BALB/c mice. Furthermore, in vivo sensitization of BALB/c mice with pRL1a MAP, but not pRL1a peptide itself, showed a marked inhibitory effect on RL♂1 tumor growth. Depletion of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated in vitro CTL generation. Selective depletion of CD4+ T cells from mice by treatment with anti-CD4 monoclonal antibody (mAb) on in vivo sensitization also abrogated in vitro CTL generation.

UR - http://www.scopus.com/inward/record.url?scp=0033302974&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033302974&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0033302974

VL - 48

SP - 61

EP - 70

JO - Gann Monographs on Cancer Research

JF - Gann Monographs on Cancer Research

SN - 0072-0151

ER -