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.

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 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.

Epstein-Barr virus isolates with the major HLA B35.01-restricted cytotoxic T lymphocyte epitope are prevalent in a highly B35.01-positive African population

1995 ◽  
Vol 25 (1) ◽  
pp. 102-110 ◽  
Author(s):  
Stefan P. Lee ◽  
Suzanne Morgan ◽  
Julia Skinner ◽  
Wendy A. Thomas ◽  
Sarah Rowland Jones ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
African Population ◽  
Barr Virus ◽  
Epstein Barr ◽  
Virus Isolates

scholarly journals Cytotoxic T-Lymphocyte Responses to a Polymorphic Epstein-Barr Virus Epitope Identify Healthy Carriers with Coresident Viral Strains

2000 ◽  
Vol 74 (4) ◽  
pp. 1801-1809 ◽  
Author(s):  
J. M. Brooks ◽  
D. S. G. Croom-Carter ◽  
A. M. Leese ◽  
R. J. Tierney ◽  
G. Habeshaw ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Distinct Type ◽  
Barr Virus ◽  
Epitope Sequence ◽  
Epstein Barr

ABSTRACT Cytotoxic T-lymphocyte (CTL) responses to Epstein-Barr virus (EBV) tend to focus on a few immunodominant viral epitopes; where these epitope sequences are polymorphic between EBV strains, host CTL specificities should reflect the identity of the resident strain. In studying responses in HLA-B27-positive virus carriers, we identified 2 of 15 individuals who had strong CTL memory to the pan-B27 epitope RRIYDLIEL (RRIY) from nuclear antigen EBNA3C but whose endogenous EBV strain, isolated in vitro, encoded a variant sequence RKIYDLIEL (RKIY) which did not form stable complexes with B27 molecules and which was poorly recognized by RRIY-specific CTLs. To check if such individuals were also carrying an epitope-positive strain (either related to or distinct from the in vitro isolate), we screened DNA from freshly isolated peripheral blood mononuclear cells for amplifiable virus sequences across the EBNA3C epitope, across a different region of EBNA3C with type 1-type 2 sequence divergence, and across a polymorphic region of EBNA1. This showed that one of the unexplained RRIY responders carried two distinct type 1 strains, one with an RKIY and one with an RRIY epitope sequence. The other responder carried an RKIY-positive type 1 strain and a type 2 virus whose epitope sequence of RRIFDLIEL was antigenically cross-reactive with RRIY. Of 15 EBV-seropositive donors analyzed by such assays, 12 appeared to be carrying a single virus strain, one was coinfected with distinct type 1 strains, and two were carrying both type 1 and type 2 viruses. This implies that a small but significant percentage of healthy virus carriers harbor multiple, perhaps sequentially acquired, EBV strains.

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