scholarly journals HLA antigen-related restriction of T lymphocyte cytotoxicity to Epstein-Barr virus.

1980 ◽  
Vol 77 (7) ◽  
pp. 4247-4250 ◽  
Author(s):  
I. S. Misko ◽  
D. J. Moss ◽  
J. H. Pope
Keyword(s):  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Hla Antigen ◽  
Barr Virus ◽  
Lymphocyte Cytotoxicity ◽  
Epstein Barr

Cytotoxic T lymphocyte responses to Epstein-Barr virus

1996 ◽  
Vol 8 (4) ◽  
pp. 492-497 ◽  
Author(s):  
Alan B Rickinson ◽  
Steven P Lee ◽  
Neil M Steven
Keyword(s):  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Barr Virus ◽  
Epstein Barr ◽  
Lymphocyte Responses

scholarly journals Association of Epstein-Barr virus with systemic lupus erythematosus: Effect modification by race, age, and cytotoxic T lymphocyte-associated antigen 4 genotype

2005 ◽  
Vol 52 (4) ◽  
pp. 1148-1159 ◽  
Author(s):  
Christine G. Parks ◽  
Glinda S. Cooper ◽  
Lori L. Hudson ◽  
Mary Anne Dooley ◽  
Edward L. Treadwell ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Lymphocyte ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Effect Modification ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals T cell-T cell killing is induced by specific epitopes: evidence for an apoptotic mechanism.

1991 ◽  
Vol 173 (3) ◽  
pp. 681-686 ◽  
Author(s):  
D J Moss ◽  
S R Burrows ◽  
G D Baxter ◽  
M F Lavin
Keyword(s):  
T Cell ◽  
T Lymphocyte ◽  
Esterase Activity ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Cell Killing ◽  
Serine Esterase ◽  
Barr Virus ◽  
Epstein Barr ◽  
Apoptotic Mechanism

Epstein-Barr virus-specific cytotoxic T lymphocyte clones were shown to be an effective target for their own lysis when incubated in the presence of their specific epitopes but not in the presence of irrelevant epitopes. The mode of cell killing appeared to be by apoptosis and was prevented by previously described inhibitors of the process. Degranulation, as measured by serine esterase activity, was involved in this form of T cell-T cell killing. This is the first report of T cell-T cell killing by apoptosis and is only observed in the presence of a specific epitope. This result may be of significance in the use of peptide-based vaccines.

scholarly journals Characterization of an human leucocyte antigen A2-restricted Epstein-Barr virus nuclear antigen-1-derived cytotoxic T-lymphocyte epitope

Immunology ◽  
2010 ◽  
Vol 129 (3) ◽  
pp. 386-395 ◽  
Author(s):  
Diego Marescotti ◽  
Federica Destro ◽  
Anna Baldisserotto ◽  
Mauro Marastoni ◽  
Giuseppe Coppotelli ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Human Leucocyte Antigen ◽  
Cytotoxic T Lymphocyte ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Epstein-Barr Virus-Induced Gene 3 (EBI3) Blocking Leads to Induce Antitumor Cytotoxic T Lymphocyte Response and Suppress Tumor Growth in Colorectal Cancer by Bidirectional Reciprocal-Regulation STAT3 Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yanfang Liang ◽  
Qianqian Chen ◽  
Wenjing Du ◽  
Can Chen ◽  
Feifei Li ◽  
...  
Keyword(s):  
Tumor Growth ◽  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Reciprocal Regulation ◽  
Barr Virus ◽  
Cell Responses ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Epstein Barr

Epstein-Barr virus-induced gene 3 (EBI3) is a member of the interleukin-12 (IL-12) family structural subunit and can form a heterodimer with IL-27p28 and IL-12p35 subunit to build IL-27 and IL-35, respectively. However, IL-27 stimulates whereas IL-35 inhibits antitumor T cell responses. To date, little is known about the role of EBI3 in tumor microenvironment. In this study, firstly we assessed EBI3, IL-27p28, IL-12p35, gp130, and p-STAT3 expression with clinicopathological parameters of colorectal cancer (CRC) tissues; then we evaluated the antitumor T cell responses and tumor growth with a EBI3 blocking peptide. We found that elevated EBI3 may be associated with IL-12p35, gp130, and p-STAT3 to promote CRC progression. EBI3 blocking peptide promoted antitumor cytotoxic T lymphocyte (CTL) response by inducing Granzyme B, IFN-γproduction, and p-STAT3 expression and inhibited CRC cell proliferation and tumor growth to associate with suppressing gp130 and p-STAT3 expression. Taken together, these results suggest that EBI3 may mediate a bidirectional reciprocal-regulation STAT3 signaling pathway to assist the tumor escape immune surveillance in CRC.

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