PMID- 9815820
OWN - NLM
STAT- MEDLINE
DCOM- 19990225
LR  - 20111117
IS  - 1078-0432 (Print)
IS  - 1078-0432 (Linking)
VI  - 3
IP  - 8
DP  - 1997 Aug
TI  - 707-AP peptide recognized by human antibody induces human leukocyte antigen 
      A2-restricted cytotoxic T lymphocyte killing of melanoma.
PG  - 1363-70
AB  - We recently identified a tumor-associated antigen that was recognized by human 
      monoclonal antibody L94. The antibody-reactive 707-AP sequence RVAALARDAP, cloned 
      from a melanoma cDNA library, was also found to be recognized by peripheral blood 
      lymphocytes (PBLs) from melanoma patients. In this study, 707-AP was used to 
      stimulate melanoma patients' PBLs for the establishment of peptide-specific CTL 
      cell lines. CTL cell lines derived from 258 melanoma patients of different human 
      leukocyte antigen (HLA)-A and HLA-B allele expressions were assessed by a 51Cr 
      cytotoxicity assay against the peptide-pulsed autologous B lymphoblastoid cells 
      and T2 HLA-A2 antigen-presenting cells and autologous and allogeneic melanoma 
      cell lines. The analysis of 707-AP CTL activity demonstrated that only HLA-A2 
      patients' PBLs could be stimulated with 707-AP. 707-AP CTLs were able to 
      specifically lyse HLA-A2 autologous and allogeneic melanoma cell lines. This 
      verified the endogenous processing and presentation of 707-AP by melanoma cells. 
      707-AP CTL cytotoxicity against peptide-pulsed autologous HLA-A2 B lymphoblastoid 
      cells and T2 HLA-A2 cells was also demonstrated. The killing activity of HLA-A2 
      707-AP CTL cell lines (CD8+ CD3+) was inhibited by anti-HLA class and anti-HLA-A2 
      monoclonal antibodies. The amino acid substitution or deletion analysis of the 
      707-AP sequence in CTL stimulation and recognition confirmed that position 2, 
      amino acid V and position 9, amino acid A were essential. Both positions are 
      known as supermotif anchors for HLA-A2 peptide sequences. Our studies 
      demonstrated that 707-AP is a potent stimulator of CTLs that can induce 
      peptide-specific HLA-A2 melanoma cell killing. The recognition of 707-AP by both 
      antibody and CTLs suggests its potential significance as a peptide 
      immunotherapeutic.
FAU - Takahashi, T
AU  - Takahashi T
AD  - Departments of Biotechnology Sciences, John Wayne Institute for Cancer Treatment 
      and Research, Santa Monica, California 90404, USA.
FAU - Irie, R F
AU  - Irie RF
FAU - Nishinaka, Y
AU  - Nishinaka Y
FAU - Hoon, D S
AU  - Hoon DS
LA  - eng
GR  - CA 12582/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Clin Cancer Res
JT  - Clinical cancer research : an official journal of the American Association for 
      Cancer Research
JID - 9502500
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (HLA-A2 Antigen)
RN  - 0 (Oligopeptides)
SB  - IM
MH  - Amino Acid Sequence
MH  - *Antibodies, Monoclonal
MH  - Antibody Specificity
MH  - Binding Sites, Antibody
MH  - *Cytotoxicity, Immunologic
MH  - HLA-A2 Antigen/*immunology
MH  - Humans
MH  - Melanoma/*immunology/pathology
MH  - Neoplasm Metastasis
MH  - Neoplasm Staging
MH  - Oligopeptides/chemical synthesis/chemistry/*immunology
MH  - Structure-Activity Relationship
MH  - T-Lymphocytes, Cytotoxic/*immunology
MH  - Tumor Cells, Cultured
EDAT- 1997/08/01 00:00
MHDA- 1998/11/17 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1998/11/17 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
PST - ppublish
SO  - Clin Cancer Res. 1997 Aug;3(8):1363-70.