PMID- 17142732
OWN - NLM
STAT- MEDLINE
DCOM- 20070116
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 177
IP  - 12
DP  - 2006 Dec 15
TI  - Latent virus influences the generation and maintenance of CD8+ T cell memory.
PG  - 8356-64
AB  - The influence of latent virus on CD8+ T cell memory is poorly understood. HSV 
      type 1 specifically establishes latency in trigeminal ganglia (TG) after corneal 
      infection of mice. In latently infected TG, IL-15 deprivation reduced the 
      following: 1) accumulation of HSV-specific CD8+ effector T cells (HSV-CD8(eff)), 
      2) accumulation of CD127(+) putative HSV-CD8 memory precursors, and 3) the size 
      and functionality of the memory (HSV-CD8(mem)) population. Although compromised 
      in IL-15(-/-) mice, the HSV-CD8(mem) pool persisted in latently infected tissue, 
      but not in noninfected tissue of the same mice. Anti-IL-2 treatment also 
      dramatically reduced the size of the HSV-CD8(eff) population in the TG, but did 
      not influence the concomitant generation of the CD127+ putative HSV-CD8(mem) 
      precursor population or the size or functionality of the HSV-CD8(mem) pool. Thus, 
      the size of the memory pool appears to be determined by the size of the CD127+ 
      CD8(mem) precursor population and not by the size of the overall CD8(eff) pool. 
      HSV-CD8(mem) showed a higher basal rate of proliferation in latently infected 
      than noninfected tissue, which was associated with a reduced population of 
      CD4+FoxP3+ regulatory T cells. Thus, the generation, maintenance, and function of 
      memory CD8+ T cells is markedly influenced by latent virus.
FAU - Sheridan, Brian S
AU  - Sheridan BS
AD  - Graduate Program in Immunology, Department of Ophthalmology, University of 
      Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
FAU - Khanna, Kamal M
AU  - Khanna KM
FAU - Frank, Gregory M
AU  - Frank GM
FAU - Hendricks, Robert L
AU  - Hendricks RL
LA  - eng
GR  - T32 AI060525/AI/NIAID NIH HHS/United States
GR  - P30 EY 08098/EY/NEI NIH HHS/United States
GR  - R01 EY005945/EY/NEI NIH HHS/United States
GR  - P30 EY008098-19/EY/NEI NIH HHS/United States
GR  - R01 EY005945-20/EY/NEI NIH HHS/United States
GR  - P30 EY008098-20/EY/NEI NIH HHS/United States
GR  - P30 EY008098-18/EY/NEI NIH HHS/United States
GR  - EY 05945/EY/NEI NIH HHS/United States
GR  - R01 EY005945-21/EY/NEI NIH HHS/United States
GR  - T32 AI 060525/AI/NIAID NIH HHS/United States
GR  - R01 EY005945-22/EY/NEI NIH HHS/United States
GR  - P30 EY008098/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Interleukin-15)
RN  - 0 (Interleukin-2)
RN  - 0 (Interleukin-7 Receptor alpha Subunit)
SB  - IM
MH  - Animals
MH  - CD8-Positive T-Lymphocytes/cytology/*immunology/virology
MH  - Cell Proliferation
MH  - Female
MH  - Herpesvirus 1, Human/immunology
MH  - *Immunologic Memory
MH  - Interleukin-15
MH  - Interleukin-2
MH  - Interleukin-7 Receptor alpha Subunit
MH  - Lymphocyte Count
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Virus Latency/*immunology
PMC - PMC2366996
MID - NIHMS47130
COIS- Disclosures The authors have no financial conflict of interest.
EDAT- 2006/12/05 09:00
MHDA- 2007/01/17 09:00
PMCR- 2008/05/05
CRDT- 2006/12/05 09:00
PHST- 2006/12/05 09:00 [pubmed]
PHST- 2007/01/17 09:00 [medline]
PHST- 2006/12/05 09:00 [entrez]
PHST- 2008/05/05 00:00 [pmc-release]
AID - 177/12/8356 [pii]
AID - 10.4049/jimmunol.177.12.8356 [doi]
PST - ppublish
SO  - J Immunol. 2006 Dec 15;177(12):8356-64. doi: 10.4049/jimmunol.177.12.8356.