Abstract
pRL1a (IPGLPLSL) is the L(d)-binding tumor rejection antigen peptide recognized by CTLs on BALB/c radiation leukemia RL♂1. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not with the pRL1a peptide itself, generated pRL1a-specific CTLs in the spleen cells of BALB/c mice. No enhancement of cytotoxicity was observed by emulsifying pRL1a MAP in incomplete Freund's adjuvant or in complete Freund's adjuvant for in vivo sensitization. Selective depletion of CD4+ T cells in mice by treatment with anti-L3T4 (CD4) monoclonal antibody and that of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated CTL generation. The findings suggest that CD4+ T cells and antigen-presenting cells were necessary for the in vivo priming of CD8+ T cells with pRL1a MAP. Furthermore, we demonstrated that in vivo sensitization of BALB/c mice with pRL1a MAP, but not with pRL1a peptide, showed an inhibitory effect on RL♂1 tumor growth. No growth-inhibitory effect was observed on control RVA, RVD, or Meth A tumors.
| Original language | English |
|---|---|
| Pages (from-to) | 1960-1964 |
| Number of pages | 5 |
| Journal | Cancer Research |
| Volume | 58 |
| Issue number | 9 |
| Publication status | Published - May 1 1998 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
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Vaccination with multiple antigen peptide as rejection antigen peptide in murine leukemia. / Manki, Akira; Ono, Toshiro; Uenaka, Akiko; Seino, Yoshiki; Nakayama, Eiichi.
In: Cancer Research, Vol. 58, No. 9, 01.05.1998, p. 1960-1964.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Vaccination with multiple antigen peptide as rejection antigen peptide in murine leukemia
AU - Manki, Akira
AU - Ono, Toshiro
AU - Uenaka, Akiko
AU - Seino, Yoshiki
AU - Nakayama, Eiichi
PY - 1998/5/1
Y1 - 1998/5/1
N2 - pRL1a (IPGLPLSL) is the L(d)-binding tumor rejection antigen peptide recognized by CTLs on BALB/c radiation leukemia RL♂1. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not with the pRL1a peptide itself, generated pRL1a-specific CTLs in the spleen cells of BALB/c mice. No enhancement of cytotoxicity was observed by emulsifying pRL1a MAP in incomplete Freund's adjuvant or in complete Freund's adjuvant for in vivo sensitization. Selective depletion of CD4+ T cells in mice by treatment with anti-L3T4 (CD4) monoclonal antibody and that of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated CTL generation. The findings suggest that CD4+ T cells and antigen-presenting cells were necessary for the in vivo priming of CD8+ T cells with pRL1a MAP. Furthermore, we demonstrated that in vivo sensitization of BALB/c mice with pRL1a MAP, but not with pRL1a peptide, showed an inhibitory effect on RL♂1 tumor growth. No growth-inhibitory effect was observed on control RVA, RVD, or Meth A tumors.
AB - pRL1a (IPGLPLSL) is the L(d)-binding tumor rejection antigen peptide recognized by CTLs on BALB/c radiation leukemia RL♂1. We demonstrated that in vivo and in vitro sensitization with pRL1a multiple antigen peptide (MAP), but not with the pRL1a peptide itself, generated pRL1a-specific CTLs in the spleen cells of BALB/c mice. No enhancement of cytotoxicity was observed by emulsifying pRL1a MAP in incomplete Freund's adjuvant or in complete Freund's adjuvant for in vivo sensitization. Selective depletion of CD4+ T cells in mice by treatment with anti-L3T4 (CD4) monoclonal antibody and that of macrophages by treatment with carrageenan on in vivo sensitization with pRL1a MAP abrogated CTL generation. The findings suggest that CD4+ T cells and antigen-presenting cells were necessary for the in vivo priming of CD8+ T cells with pRL1a MAP. Furthermore, we demonstrated that in vivo sensitization of BALB/c mice with pRL1a MAP, but not with pRL1a peptide, showed an inhibitory effect on RL♂1 tumor growth. No growth-inhibitory effect was observed on control RVA, RVD, or Meth A tumors.
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M3 - Article
C2 - 9581839
AN - SCOPUS:0032080639
VL - 58
SP - 1960
EP - 1964
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0008-5472
IS - 9
ER -