PMID- 19689735
OWN - NLM
STAT- MEDLINE
DCOM- 20091104
LR  - 20211020
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 128
IP  - 1
DP  - 2009 Sep
TI  - Lentiviral calnexin-modified dendritic cells promote expansion of high-avidity 
      effector T cells with central memory phenotype.
PG  - 43-57
LID - 10.1111/j.1365-2567.2009.03067.x [doi]
AB  - Dendritic cells (DCs) are key immune mediators for the education and activation 
      of effector cytotoxic T lymphocytes (CTLs). Ex vivo manipulation of DCs is an 
      attractive strategy in immunotherapy. The chaperone proteins are known to hold 
      the keys to proper protein folding and antigen processing. However, little is 
      known of the role of molecular chaperones in DC and T-cell functions. We report 
      that DCs expressing supraphysiological levels of calnexin, a chaperone protein, 
      via lentiviral gene transfer stimulated the expansion of high-avidity CTLs with 
      increased central memory phenotype. Microarray RNA profiling and analyses of 
      protein expression with flow cytometry and multiplex enzyme-linked immunosorbent 
      assay indicated that calnexin had a global effect on DCs with up-regulation of 
      immune modulatory signals including costimulatory molecules, cytokines, 
      chemokines and adhesion molecules. Compared with unmodified DCs, calnexin-DCs 
      were capable of activating T cells to exhibit increased functional avidity 
      associated with up-regulation of CCR7 and costimulatory tumour necrosis factor 
      receptor superfamily molecules. These findings demonstrate a prominent role of 
      calnexin in optimizing DC immunity with potential for improving immunotherapy.
FAU - Wang, Bei
AU  - Wang B
AD  - Department of Molecular Genetics and Microbiology, University of Florida, College 
      of Medicine, Gainesville, FL, USA.
FAU - Han, Shuhong
AU  - Han S
FAU - Lien, Lily
AU  - Lien L
FAU - Chang, Lung-Ji
AU  - Chang LJ
LA  - eng
GR  - P01 HL059412/HL/NHLBI NIH HHS/United States
GR  - P50 HL059412/HL/NHLBI NIH HHS/United States
GR  - HL59412/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Cancer Vaccines)
RN  - 0 (Ccr7 protein, mouse)
RN  - 0 (Receptors, CCR7)
RN  - 139873-08-8 (Calnexin)
SB  - IM
MH  - Animals
MH  - Antibody Affinity
MH  - Antigen Presentation/immunology
MH  - Calnexin/*immunology
MH  - Cancer Vaccines/therapeutic use
MH  - Cell Proliferation
MH  - Coculture Techniques
MH  - Colonic Neoplasms/therapy
MH  - Dendritic Cells/*immunology/transplantation
MH  - Genetic Vectors
MH  - Immunologic Memory
MH  - Immunophenotyping
MH  - Lentivirus/genetics
MH  - Lymphocyte Activation/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Receptors, CCR7/metabolism
MH  - T-Lymphocytes, Cytotoxic/*immunology
MH  - Transduction, Genetic
MH  - Tumor Cells, Cultured
PMC - PMC2747138
EDAT- 2009/08/20 09:00
MHDA- 2009/11/05 06:00
PMCR- 2010/09/01
CRDT- 2009/08/20 09:00
PHST- 2009/08/20 09:00 [entrez]
PHST- 2009/08/20 09:00 [pubmed]
PHST- 2009/11/05 06:00 [medline]
PHST- 2010/09/01 00:00 [pmc-release]
AID - IMM3067 [pii]
AID - 10.1111/j.1365-2567.2009.03067.x [doi]
PST - ppublish
SO  - Immunology. 2009 Sep;128(1):43-57. doi: 10.1111/j.1365-2567.2009.03067.x.