PMID- 21087352
OWN - NLM
STAT- MEDLINE
DCOM- 20110118
LR  - 20210103
IS  - 1349-7006 (Electronic)
IS  - 1347-9032 (Linking)
VI  - 102
IP  - 1
DP  - 2011 Jan
TI  - Peptides derived from human insulin-like growth factor-II mRNA binding protein 3 
      can induce human leukocyte antigen-A2-restricted cytotoxic T lymphocytes reactive 
      to cancer cells.
PG  - 71-8
LID - 10.1111/j.1349-7006.2010.01780.x [doi]
AB  - Insulin-like growth factor-II mRNA binding protein 3 (IMP-3) is an oncofetal 
      protein expressed in various malignancies including lung cancer. This study aimed 
      to identify immunogenic peptides derived from IMP-3 that can induce 
      tumor-reactive and human leukocyte antigen (HLA)-A2 (A*02:01)-restricted 
      cytotoxic T lymphocytes (CTL) for lung cancer immunotherapy. Forty human 
      IMP-3-derived peptides predicted to bind to HLA-A2 were analyzed to determine 
      their capacity to induce HLA-A2-restricted T cells in HLA-A2.1 (HHD) transgenic 
      mice (Tgm). We found that three IMP-3 peptides primed HLA-A2-restricted CTL in 
      the HLA-A2.1 Tgm. Among them, human CTL lines reactive to IMP-3 (515) 
      NLSSAEVVV(523) were reproducibly established from HLA-A2-positive healthy donors 
      and lung cancer patients. On the other hand, IMP-3 (199) RLLVPTQFV(207) 
      reproducibly induced IMP-3-specific and HLA-A2-restricted CTL from healthy 
      donors, but did not sensitize CTL in the HLA-A2.1 Tgm. Importantly, these two 
      IMP-3 peptide-specific CTL generated from healthy donors and cancer patients 
      effectively killed the cancer cells naturally expressing both IMP-3 and HLA-A2. 
      Cytotoxicity was significantly inhibited by anti-HLA class I and anti-HLA-A2 
      monoclonal antibodies, but not by the anti-HLA-class II monoclonal antibody. In 
      addition, natural processing of these two epitopes derived from the IMP-3 protein 
      was confirmed by specific killing of HLA-A2-positive IMP-3-transfectants but not 
      the parental IMP-negative cell line by peptide-induced CTL. This suggests that 
      these two IMP-3-derived peptides represent highly immunogenic CTL epitopes that 
      may be attractive targets for lung cancer immunotherapy.
CI  - (c) 2010 Japanese Cancer Association.
FAU - Tomita, Yusuke
AU  - Tomita Y
AD  - Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto 
      University, Kumamoto, Japan.
FAU - Harao, Michiko
AU  - Harao M
FAU - Senju, Satoru
AU  - Senju S
FAU - Imai, Katsunori
AU  - Imai K
FAU - Hirata, Shinya
AU  - Hirata S
FAU - Irie, Atsushi
AU  - Irie A
FAU - Inoue, Mitsuhiro
AU  - Inoue M
FAU - Hayashida, Yuki
AU  - Hayashida Y
FAU - Yoshimoto, Kentaro
AU  - Yoshimoto K
FAU - Shiraishi, Kenji
AU  - Shiraishi K
FAU - Mori, Takeshi
AU  - Mori T
FAU - Nomori, Hiroaki
AU  - Nomori H
FAU - Kohrogi, Hirotsugu
AU  - Kohrogi H
FAU - Nishimura, Yasuharu
AU  - Nishimura Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101119
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (HLA-A2 Antigen)
RN  - 0 (IGF2BP3 protein, human)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA-Binding Proteins)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Epitopes, T-Lymphocyte
MH  - HLA-A2 Antigen/*immunology
MH  - Humans
MH  - Lung Neoplasms/immunology
MH  - Mice
MH  - Neoplasms/*immunology
MH  - Peptide Fragments/*immunology
MH  - RNA-Binding Proteins/genetics/*immunology
MH  - T-Lymphocytes, Cytotoxic/*immunology
EDAT- 2010/11/23 06:00
MHDA- 2011/01/19 06:00
CRDT- 2010/11/20 06:00
PHST- 2010/11/20 06:00 [entrez]
PHST- 2010/11/23 06:00 [pubmed]
PHST- 2011/01/19 06:00 [medline]
AID - 10.1111/j.1349-7006.2010.01780.x [doi]
PST - ppublish
SO  - Cancer Sci. 2011 Jan;102(1):71-8. doi: 10.1111/j.1349-7006.2010.01780.x. Epub 
      2010 Nov 19.