PMID- 18840303
OWN - NLM
STAT- MEDLINE
DCOM- 20081202
LR  - 20181113
IS  - 1742-4690 (Electronic)
IS  - 1742-4690 (Linking)
VI  - 5
DP  - 2008 Oct 8
TI  - Activation and detection of HTLV-I Tax-specific CTLs by epitope expressing 
      single-chain trimers of MHC class I in a rat model.
PG  - 90
LID - 10.1186/1742-4690-5-90 [doi]
AB  - BACKGROUND: Human T cell leukemia virus type I (HTLV-I) causes adult T-cell 
      leukemia (ATL) in infected individuals after a long incubation period. 
      Immunological studies have suggested that insufficient host T cell response to 
      HTLV-I is a potential risk factor for ATL. To understand the relationship between 
      host T cell response and HTLV-I pathogenesis in a rat model system, we have 
      developed an activation and detection system of HTLV-I Tax-specific cytotoxic T 
      lymphocytes (CTLs) by Epitope expressing Single-Chain Trimers (SCTs) of MHC class 
      I. RESULTS: We have established expression vectors which encode SCTs of rat MHC-I 
      (RT1.Al) with Tax180-188 peptide. Human cell lines transfected with the 
      established expression vectors were able to induce IFN-gamma and TNF-alpha 
      production by a Tax180-188-specific CTL line, 4O1/C8. We have further fused the 
      C-terminus of SCTs to EGFP and established cells expressing SCT-EGFP fusion 
      protein on the surface. By co-cultivating the cells with 4O1/C8, we have 
      confirmed that the epitope-specific CTLs acquired SCT-EGFP fusion proteins and 
      that these EGFP-possessed CTLs were detectable by flow cytometric analysis. 
      CONCLUSION: We have generated a SCT of rat MHC-I linked to Tax epitope peptide, 
      which can be applicable for the induction of Tax-specific CTLs in rat model 
      systems of HTLV-I infection. We have also established a detection system of 
      Tax-specific CTLs by using cells expressing SCTs fused with EGFP. These systems 
      will be useful tools in understanding the role of HTLV-I specific CTLs in HTLV-I 
      pathogenesis.
FAU - Ohashi, Takashi
AU  - Ohashi T
AD  - Division of Molecular Virology, Institute for Genetic Medicine, Hokkaido 
      University, Sapporo, Japan. ohashi-t@igm.hokudai.ac.jp
FAU - Nagai, Mika
AU  - Nagai M
FAU - Okada, Hiroyuki
AU  - Okada H
FAU - Takayanagi, Ryo
AU  - Takayanagi R
FAU - Shida, Hisatoshi
AU  - Shida H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081008
PL  - England
TA  - Retrovirology
JT  - Retrovirology
JID - 101216893
RN  - 0 (Cytokines)
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (Gene Products, tax)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (tax protein, Human T-lymphotrophic virus 1)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Cell Line
MH  - Cells, Cultured
MH  - Cytokines/genetics/immunology
MH  - Disease Models, Animal
MH  - Epitopes, T-Lymphocyte/*genetics/immunology
MH  - Female
MH  - *Gene Expression
MH  - Gene Products, tax/*genetics/immunology
MH  - *Genes, MHC Class I
MH  - Genetic Vectors/genetics
MH  - HTLV-I Infections/*immunology/virology
MH  - Human T-lymphotropic virus 1/*genetics/immunology
MH  - Humans
MH  - Leukemia-Lymphoma, Adult T-Cell/immunology/virology
MH  - Molecular Sequence Data
MH  - Rats
MH  - Rats, Inbred F344
MH  - Recombinant Fusion Proteins/genetics/immunology
MH  - T-Lymphocytes, Cytotoxic/*immunology/virology
MH  - *Transcriptional Activation
PMC - PMC2579301
EDAT- 2008/10/09 09:00
MHDA- 2008/12/17 09:00
PMCR- 2008/10/08
CRDT- 2008/10/09 09:00
PHST- 2008/07/22 00:00 [received]
PHST- 2008/10/08 00:00 [accepted]
PHST- 2008/10/09 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/10/09 09:00 [entrez]
PHST- 2008/10/08 00:00 [pmc-release]
AID - 1742-4690-5-90 [pii]
AID - 10.1186/1742-4690-5-90 [doi]
PST - epublish
SO  - Retrovirology. 2008 Oct 8;5:90. doi: 10.1186/1742-4690-5-90.