PMID- 18509087
OWN - NLM
STAT- MEDLINE
DCOM- 20081030
LR  - 20211020
IS  - 1528-0020 (Electronic)
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 112
IP  - 6
DP  - 2008 Sep 15
TI  - Retrovirally induced CTL degranulation mediated by IL-15 expression and infection 
      of mononuclear phagocytes in patients with HTLV-I-associated neurologic disease.
PG  - 2400-10
LID - 10.1182/blood-2008-02-138529 [doi]
AB  - CD8(+) T cells contribute to central nervous system inflammation in human T-cell 
      lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic 
      paraparesis (HAM/TSP). We analyzed CD8(+) T-cell dysfunction (degranulation and 
      IFN-gamma production) and have demonstrated that CD8(+) T cells of patients with 
      HAM/TSP (HAM/TSP patients) spontaneously degranulate and express IFN-gamma in ex 
      vivo unstimulated culture. CD8(+) T cells of HTLV-I asymptomatic carriers and 
      healthy donors did not. Spontaneous degranulation was detected in 
      Tax11-19/HLA-A*201 tetramer(+) cells, but not in CMV pp65 tetramer(+) cells. 
      Interestingly, degranulation and IFN-gamma production in CD8(+) T cells was 
      induced by coculture with autologous CD14(+) cells, but not CD4(+) T cells, of 
      HAM/TSP patients, which correlated with proviral DNA load in CD14(+) cells of 
      infected patients. Moreover, the expression of IL-15, which induced degranulation 
      and IFN-gamma production in infected patients, was enhanced on surface of CD14(+) 
      cells in HAM/TSP patients. Blockade of MHC class I and IL-15 confirmed these 
      results. Thus, CD8(+) T-cell dysregulation was mediated by both virus infection 
      and enhanced IL-15 on CD14(+) cells in HAM/TSP patients. Despite lower viral 
      expression than in CD4(+) T cells, HTLV-I-infected or -activated CD14(+) cells 
      may be a heretofore important but under recognized reservoir particularly in 
      HAM/TSP patients.
FAU - Enose-Akahata, Yoshimi
AU  - Enose-Akahata Y
AD  - Viral Immunology Section, Neuroimmunology Branch, National Institute of 
      Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 
      20892, USA.
FAU - Oh, Unsong
AU  - Oh U
FAU - Grant, Christian
AU  - Grant C
FAU - Jacobson, Steven
AU  - Jacobson S
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20080528
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Interleukin-15)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - CD8-Positive T-Lymphocytes/virology
MH  - *Cell Degranulation
MH  - Coculture Techniques
MH  - Gene Expression/immunology
MH  - HTLV-I Infections
MH  - Human T-lymphotropic virus 1/*pathogenicity
MH  - Humans
MH  - Interferon-gamma/genetics
MH  - Interleukin-15/*genetics
MH  - Lipopolysaccharide Receptors/analysis
MH  - Paraparesis, Tropical Spastic/*virology
MH  - Phagocytes/*virology
MH  - T-Lymphocytes, Cytotoxic/*virology
PMC - PMC2532810
EDAT- 2008/05/30 09:00
MHDA- 2008/10/31 09:00
PMCR- 2009/09/15
CRDT- 2008/05/30 09:00
PHST- 2008/05/30 09:00 [pubmed]
PHST- 2008/10/31 09:00 [medline]
PHST- 2008/05/30 09:00 [entrez]
PHST- 2009/09/15 00:00 [pmc-release]
AID - S0006-4971(20)59863-7 [pii]
AID - 2008/138529 [pii]
AID - 10.1182/blood-2008-02-138529 [doi]
PST - ppublish
SO  - Blood. 2008 Sep 15;112(6):2400-10. doi: 10.1182/blood-2008-02-138529. Epub 2008 
      May 28.