PMID- 16424200
OWN - NLM
STAT- MEDLINE
DCOM- 20060324
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 176
IP  - 3
DP  - 2006 Feb 1
TI  - Qa-1b and CD94-NKG2a interaction regulate cytolytic activity of herpes simplex 
      virus-specific memory CD8+ T cells in the latently infected trigeminal ganglia.
PG  - 1703-11
AB  - After ocular infection, HSV-specific CD8+ T cells migrate to and are specifically 
      retained in the ophthalmic branch of the trigeminal ganglia (TG) even at the time 
      when replicating virus is no longer evident. Virus-specific CD8+ T cells maintain 
      an activation phenotype and secrete IFN-gamma in the latent TG. In this report we 
      demonstrated that activated virus-specific memory CD8+ T cells, although 
      potentially cytolytic, also expressed the CD94-NK cell receptor subfamily G2a 
      inhibitory molecule and were unable to exert cytotoxicity when engaged by Qa-1b 
      expressing targets. Interestingly, many neurons in the latent TG expressed Qa-1b, 
      and blocking of Qa-1b/CD94-NKG2a interaction in an ex vivo TG culture resulted in 
      neuronal cell lysis. The expression of the inhibitory CD94-NKG2a molecule could 
      be induced by TGF-beta1, which was shown to present as a bioactive molecule in 
      the latent TG. Additionally, CD4+ forkhead/winged helix transcription factor 3+ T 
      cells were also determined in the latent TG. Our results demonstrate the 
      operation of a regulatory system in vivo that serves to protect irreplaceable 
      neurons from destruction by the immune system.
FAU - Suvas, Susmit
AU  - Suvas S
AD  - Department of Microbiology, University of Tennessee, Knoxville, TN 37996, USA. 
      ssuvas@utk.edu
FAU - Azkur, Ahmet Kursat
AU  - Azkur AK
FAU - Rouse, Barry T
AU  - Rouse BT
LA  - eng
GR  - AI114981/AI/NIAID NIH HHS/United States
GR  - EYO5093/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Foxp3 protein, mouse)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Klrc1 protein, mouse)
RN  - 0 (NK Cell Lectin-Like Receptor Subfamily C)
RN  - 0 (NK Cell Lectin-Like Receptor Subfamily D)
RN  - 0 (Q surface antigens)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Natural Killer Cell)
SB  - IM
MH  - Animals
MH  - CD8-Positive T-Lymphocytes/*immunology/virology
MH  - Cells, Cultured
MH  - *Cytotoxicity, Immunologic
MH  - Epitopes, T-Lymphocyte/immunology
MH  - Female
MH  - Forkhead Transcription Factors/metabolism
MH  - Histocompatibility Antigens Class I/*physiology
MH  - *Immunologic Memory
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NK Cell Lectin-Like Receptor Subfamily C
MH  - NK Cell Lectin-Like Receptor Subfamily D/*physiology
MH  - Receptors, Immunologic/*physiology
MH  - Receptors, Natural Killer Cell
MH  - Simplexvirus/*immunology
MH  - T-Lymphocytes, Regulatory/metabolism
MH  - Trigeminal Ganglion/cytology/*immunology/metabolism/virology
MH  - Virus Latency/immunology
EDAT- 2006/01/21 09:00
MHDA- 2006/03/25 09:00
CRDT- 2006/01/21 09:00
PHST- 2006/01/21 09:00 [pubmed]
PHST- 2006/03/25 09:00 [medline]
PHST- 2006/01/21 09:00 [entrez]
AID - 176/3/1703 [pii]
AID - 10.4049/jimmunol.176.3.1703 [doi]
PST - ppublish
SO  - J Immunol. 2006 Feb 1;176(3):1703-11. doi: 10.4049/jimmunol.176.3.1703.