PMID- 10666215
OWN - NLM
STAT- MEDLINE
DCOM- 20000314
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 95
IP  - 4
DP  - 2000 Feb 15
TI  - Abundant tax protein expression in CD4+ T cells infected with human T-cell 
      lymphotropic virus type I (HTLV-I) is prevented by cytotoxic T lymphocytes.
PG  - 1386-92
AB  - The role of the cellular immune response in human T-cell leukemia virus type I 
      (HTLV-I) infection is not fully understood. A persistently activated cytotoxic T 
      lymphocyte (CTL) response to HTLV-I is found in the majority of infected 
      individuals. However, it remains unclear whether this CTL response is protective 
      or causes tissue damage. In addition, several observations paradoxically suggest 
      that HTLV-I is transcriptionally silent in most infected cells and, therefore, 
      not detectable by virus-specific CTLs. With the use of a new flow cytometric 
      procedure, we show here that a high proportion of naturally infected CD4+ 
      peripheral blood mononuclear cells (PBMC) (between 10% and 80%) are capable of 
      expressing Tax, the immunodominant target antigen recognized by virus-specific 
      CTLs. Furthermore, we provide direct evidence that autologous CD8+ T cells 
      rapidly kill CD4+ cells naturally infected with HTLV-I and expressing Tax in 
      vitro by a perforin-dependent mechanism. Consistent with these observations, we 
      observed a significant negative correlation between the frequency of 
      Tax(11-19)-specific CD8+ T cells and the percentage of CD4+ T cells in peripheral 
      blood of patients infected with HTLV-I. Those results are in accordance with the 
      view that virus-specific CTLs participate in a highly efficient immune 
      surveillance mechanism that persistently destroys Tax-expressing HTLV-I-infected 
      CD4+ T cells in vivo. (Blood. 2000;95:1386-1392)
FAU - Hanon, E
AU  - Hanon E
AD  - Department of Immunology and Genito-Urinary Medicine and Communicable Diseases, 
      Imperial College School of Medicine, St Mary's Campus, London, United Kingdom.
FAU - Hall, S
AU  - Hall S
FAU - Taylor, G P
AU  - Taylor GP
FAU - Saito, M
AU  - Saito M
FAU - Davis, R
AU  - Davis R
FAU - Tanaka, Y
AU  - Tanaka Y
FAU - Usuku, K
AU  - Usuku K
FAU - Osame, M
AU  - Osame M
FAU - Weber, J N
AU  - Weber JN
FAU - Bangham, C R
AU  - Bangham CR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (Antiviral Agents)
RN  - 0 (Gene Products, tax)
RN  - 0 (Macrolides)
RN  - 0 (RNA, Messenger)
RN  - 80890-47-7 (concanamycin A)
SB  - IM
MH  - Anti-Bacterial Agents/pharmacology
MH  - Antiviral Agents/pharmacology
MH  - CD4-Positive T-Lymphocytes/*immunology/*virology
MH  - Cell Line
MH  - Cells, Cultured
MH  - Flow Cytometry
MH  - Gene Expression Regulation, Viral/drug effects/*immunology
MH  - Gene Products, tax/*genetics
MH  - Human T-lymphotropic virus 1/*genetics/immunology
MH  - Humans
MH  - Kinetics
MH  - Lymphocyte Activation
MH  - *Macrolides
MH  - Paraparesis, Tropical Spastic/*immunology
MH  - RNA, Messenger/genetics
MH  - T-Lymphocytes, Cytotoxic/*immunology/*virology
MH  - Transcription, Genetic
EDAT- 2000/02/09 09:00
MHDA- 2000/03/18 09:00
CRDT- 2000/02/09 09:00
PHST- 2000/02/09 09:00 [pubmed]
PHST- 2000/03/18 09:00 [medline]
PHST- 2000/02/09 09:00 [entrez]
AID - S0006-4971(20)67088-4 [pii]
PST - ppublish
SO  - Blood. 2000 Feb 15;95(4):1386-92.