PMID- 17545629
OWN - NLM
STAT- MEDLINE
DCOM- 20070726
LR  - 20210102
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 67
IP  - 11
DP  - 2007 Jun 1
TI  - Expression and functional analysis of human leukocyte antigen class I 
      antigen-processing machinery in medulloblastoma.
PG  - 5471-8
AB  - Defects in the expression and/or function of the human leukocyte antigen (HLA) 
      class I antigen-processing machinery (APM) components are found in many tumor 
      types. These abnormalities may have a negative impact on the interactions of 
      tumor cells with host's immune system and on the outcome of T cell-based 
      immunotherapy. To the best of our knowledge, no information is available about 
      APM component expression and functional characteristics in human medulloblastoma 
      cells (Mb). Therefore, in the present study, we have initially compared the 
      expression of APM components in Mb, an embryonal pediatric brain tumor with a 
      poor prognosis, with that in noninfiltrating astrocytic pediatric tumors, a group 
      of differentiated brain malignancies with favorable prognosis. LMP2, LMP7, 
      calnexin, beta2-microglobulin-free heavy chain (HC) and beta2-microglobulin were 
      down-regulated or undetectable in Mb lesions, but not in astrocytic tumors or 
      normal fetal cerebellum. Two Mb cell lines (DAOI and D283) displayed similar but 
      not superimposable defects in APM component expression as compared with primary 
      tumors. To assess the functional implications of HLA class I APM component 
      down-regulation in Mb cell lines, we tested their recognition by HLA class I 
      antigen-restricted, tumor antigen (TA)-specific CTL, generated by stimulations 
      with dendritic cells that had been transfected with Mb mRNA. The Mb cell lines 
      were lysed by TA-specific CTL in a HLA-restricted manner. Thus, defective 
      expression of HLA class I-related APM components in Mb cells does not impair 
      their ability to present TA to TA-specific CTL. In conclusion, these results can 
      contribute to optimize T cell-based immunotherapeutic strategies for Mb 
      treatment.
FAU - Raffaghello, Lizzia
AU  - Raffaghello L
AD  - Laboratories of Oncology, G. Gaslini Institute, Genoa, Italy. 
      lizziaraffaghello@ospedale-gaslini.ge.it
FAU - Nozza, Paolo
AU  - Nozza P
FAU - Morandi, Fabio
AU  - Morandi F
FAU - Camoriano, Marta
AU  - Camoriano M
FAU - Wang, Xinhui
AU  - Wang X
FAU - Garre, Maria Luisa
AU  - Garre ML
FAU - Cama, Armando
AU  - Cama A
FAU - Basso, Giuseppe
AU  - Basso G
FAU - Ferrone, Soldano
AU  - Ferrone S
FAU - Gambini, Claudio
AU  - Gambini C
FAU - Pistoia, Vito
AU  - Pistoia V
LA  - eng
GR  - R01 CA110249/CA/NCI NIH HHS/United States
GR  - R01 CA113861/CA/NCI NIH HHS/United States
GR  - R01 CA67108/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (HLA-A Antigens)
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA-C Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
MH  - Antigen Presentation
MH  - Brain Neoplasms/*immunology
MH  - Cell Line, Tumor
MH  - Child
MH  - Child, Preschool
MH  - Female
MH  - HLA-A Antigens/biosynthesis/immunology
MH  - HLA-B Antigens/biosynthesis/immunology
MH  - HLA-C Antigens/biosynthesis/immunology
MH  - Histocompatibility Antigens Class I/biosynthesis/*immunology
MH  - Humans
MH  - Male
MH  - Medulloblastoma/*immunology
MH  - T-Lymphocytes/immunology
EDAT- 2007/06/05 09:00
MHDA- 2007/07/27 09:00
CRDT- 2007/06/05 09:00
PHST- 2007/06/05 09:00 [pubmed]
PHST- 2007/07/27 09:00 [medline]
PHST- 2007/06/05 09:00 [entrez]
AID - 67/11/5471 [pii]
AID - 10.1158/0008-5472.CAN-06-4735 [doi]
PST - ppublish
SO  - Cancer Res. 2007 Jun 1;67(11):5471-8. doi: 10.1158/0008-5472.CAN-06-4735.