PMID- 12973031
OWN - NLM
STAT- MEDLINE
DCOM- 20040409
LR  - 20210102
IS  - 1524-9557 (Print)
IS  - 1524-9557 (Linking)
VI  - 26
IP  - 5
DP  - 2003 Sep-Oct
TI  - Enhancement of antigen-presenting capacity and antitumor immunity of dendritic 
      cells pulsed with autologous tumor-derived RNA in mice.
PG  - 420-31
AB  - Dendritic cells (DCs) are antigen-presenting cells that play an important role in 
      antitumor immunity. Several studies have reported that DCs pulsed with RNA from 
      tumor cells have the ability to suppress tumors, but the details regarding the 
      function and the immune-mechanism of DCs transfected with RNA remain to be 
      elucidated. In this study, we investigated the transfection efficiency of RNA 
      into DCs, and the functional modification and the antitumor efficacy of DCs 
      pulsed with tumor-derived RNA. After the transfection of tumor-derived RNA into 
      DCs cultured from the bone marrow of mice, pulsed DCs exhibited a high expression 
      of both MHC antigens and CD86 on the cell surface as well as cultured DCs, and 
      had a stronger ability both to present antigen on the MHC antigens and to 
      stimulate T cells compared with DCs without transfection. DCs could sufficiently 
      translate luciferase encoding RNA into luciferase proteins, and luciferase 
      protein was expressed up to 12 hours in pulsed DCs. The DCs pulsed with 
      tumor-derived RNA could elite a potent induction of cytotoxic T lymphocytes 
      against autologous tumors, but not lysis against syngeneic normal cells. 
      RNA-pulsed DCs exhibited a significant antitumor immunity in animal model. In 
      conclusion, DCs could sufficiently uptake exogenous tumor-derived RNA, and 
      consequently grow to be an intermediate maturate type, and induce potent T-cell 
      stimulation and fully cause an antitumor effect in vivo. Therapy with DCs pulsed 
      with tumor-derived RNA is sufficiently effective and safe, and thus it is 
      considered to be clinically useful for tumor-immunotherapy.
FAU - Minami, Takahiro
AU  - Minami T
AD  - Research Institute for Diseases of the Chest, Graduate School of Medical 
      Sciences, Kyushu University, Maidashi, Higashiku, Fukuoka, Japan.
FAU - Nakanishi, Yoichi
AU  - Nakanishi Y
FAU - Izumi, Miiru
AU  - Izumi M
FAU - Harada, Taishi
AU  - Harada T
FAU - Hara, Nobuyuki
AU  - Hara N
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Immunother
JT  - Journal of immunotherapy (Hagerstown, Md. : 1997)
JID - 9706083
RN  - 0 (RNA, Neoplasm)
RN  - EC 2.7.7.6 (DNA-Directed RNA Polymerases)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - *Antigen Presentation
MH  - Bone Marrow Cells/cytology
MH  - Carcinoma, Lewis Lung
MH  - Cell Differentiation
MH  - Cell Line, Tumor
MH  - Cells, Cultured
MH  - DNA-Directed RNA Polymerases/genetics
MH  - Dendritic Cells/*immunology
MH  - Endocytosis
MH  - Female
MH  - Genes, Reporter
MH  - Immunotherapy, Adoptive/*methods
MH  - Lymphocyte Activation
MH  - Melanoma, Experimental
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Neoplasms, Experimental/*therapy
MH  - *RNA, Neoplasm
MH  - T-Lymphocytes, Cytotoxic/immunology
MH  - Transfection
EDAT- 2003/09/16 05:00
MHDA- 2004/04/10 05:00
CRDT- 2003/09/16 05:00
PHST- 2003/09/16 05:00 [pubmed]
PHST- 2004/04/10 05:00 [medline]
PHST- 2003/09/16 05:00 [entrez]
AID - 10.1097/00002371-200309000-00005 [doi]
PST - ppublish
SO  - J Immunother. 2003 Sep-Oct;26(5):420-31. doi: 10.1097/00002371-200309000-00005.