Recognition of Epstein-Barr virus-associated gastric carcinoma cells by cytotoxic T lymphocytes induced in vitro with autologous lymphoblastoid cell line and LMP2-derived, HLA-A24-restricted 9-mer peptide

2004 ◽  
Author(s):  
Kaori Okugawa ◽  
Tsuyoshi Itoh ◽  
Ichiro Kawashima ◽  
Kazutoh Takesako ◽  
Osam Mazda ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Gastric Carcinoma ◽  
Cell Line ◽  
Cytotoxic T Lymphocytes ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Carcinoma Cells ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals An Epstein-Barr Virus Isolated from a Lymphoblastoid Cell Line Has a 16-Kilobase-Pair Deletion Which Includes gp350 and the Epstein-Barr Virus Nuclear Antigen 3A

2001 ◽  
Vol 75 (18) ◽  
pp. 8556-8568 ◽  
Author(s):  
Wonkeun Lee ◽  
Yoon-Ha Hwang ◽  
Suk-Kyeong Lee ◽  
Chitra Subramanian ◽  
Erle S. Robertson
Keyword(s):  
Cell Line ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Lymphoblastoid Cell Line ◽  
Phorbol Esters ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Amino Terminal ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) is associated with human cancers, including nasopharyngeal carcinoma, Burkitt's lymphoma, gastric carcinoma and, somewhat controversially, breast carcinoma. EBV infects and efficiently transforms human primary B lymphocytes in vitro. A number of EBV-encoded genes are critical for EBV-mediated transformation of human B lymphocytes. In this study we show that an EBV-infected lymphoblastoid cell line obtained from the spontaneous outgrowth of B cells from a leukemia patient contains a deletion, which involves a region of approximately 16 kbp. This deletion encodes major EBV genes involved in both infection and transformation of human primary B lymphocytes and includes the glycoprotein gp350, the entire open reading frame of EBNA3A, and the amino-terminal region of EBNA3B. A fusion protein created by this deletion, which lies between the BMRF1 early antigen and the EBNA3B latent antigen, is truncated immediately downstream of the junction 21 amino acids into the region of the EBNA3B sequence, which is out of frame with respect to the EBNA3B protein sequence, and indicates that EBNA3B is not expressed. The fusion is from EBV coordinate 80299 within the BMRF1 sequence to coordinate 90998 in the EBNA3B sequence. Additionally, we have shown that there is no detectable induction in viral replication observed when SNU-265 is treated with phorbol esters, and no transformants were detected when supernatant is used to infect primary B lymphocytes after 8 weeks in culture. Therefore, we have identified an EBV genome with a major deletion in critical genes involved in mediating EBV infection and the transformation of human primary B lymphocytes that is incompetent for replication of this naturally occurring EBV isolate.

scholarly journals Increased frequency of antigen-specific CD8+ cytotoxic T lymphocytes infiltrating an Epstein-Barr virus–associated gastric carcinoma

1999 ◽  
Vol 104 (2) ◽  
pp. 163-171 ◽  
Author(s):  
Kiyotaka Kuzushima ◽  
Shigeo Nakamura ◽  
Tsuneya Nakamura ◽  
Yoshitaka Yamamura ◽  
Naoaki Yokoyama ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Gastric Carcinoma ◽  
Cytotoxic T Lymphocytes ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Development of suppressor T lymphocytes for Epstein-Barr virus-induced B-lymphocyte outgrowth during acute infectious mononucleosis: assessment by two quantitative systems

Blood ◽  
1981 ◽  
Vol 57 (3) ◽  
pp. 510-517 ◽  
Author(s):  
RT Schooley ◽  
BF Haynes ◽  
J Grouse ◽  
C Payling-Wright ◽  
AS Fauci ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
B Lymphocyte ◽  
Acute Stage ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Epstein Barr

Abstract A system of 3H-thymidine incorporation by lymphocytes in culture for 3 wk has been utilized for quantitative assessment of the ability of T lymphocytes to inhibit outgrowth of autologous Epstein-Barr virus (EBV) transformed B lymphocytes. Lymphocytes from EBV-seronegative individuals lack the ability to suppress outgrowth of autologous EBV- transformed B lymphocytes. This capability appears during the course of primary EBV-induced infectious mononucleases (IM) as the atypical lymphocytosis is subsiding and persists for years after recovery from primary EBV infection. The ability of T lymphocytes from EBV- seropositive subjects or convalescent IM patients to inhibit B- lymphocyte outgrowth is not HLA restricted. Thus, T lymphocytes capable of inhibition of in vitro EBV-induced B-cell outgrowth emerge during the acute stage of IM and may represent an important control mechanism of EBV-induced B-lymphocyte proliferation in vivo. The system provides a highly sensitive quantitative means for in vitro assessment of cell- mediated immunity to EBV.

scholarly journals Epstein-Barr Virus-Encoded BARF1 Promotes Proliferation of Gastric Carcinoma Cells through Regulation of NF- B

2013 ◽  
Vol 87 (19) ◽  
pp. 10515-10523 ◽  
Author(s):  
M. S. Chang ◽  
D. H. Kim ◽  
J. K. Roh ◽  
J. M. Middeldorp ◽  
Y. S. Kim ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
Carcinoma Cells ◽  
Barr Virus ◽  
Epstein Barr

Longitudinal dynamics of antigen-specific CD8+cytotoxic T lymphocytes following primary Epstein-Barr virus infection

Blood ◽  
2001 ◽  
Vol 98 (8) ◽  
pp. 2588-2589 ◽  
Author(s):  
Mandvi Bharadwaj ◽  
Scott R. Burrows ◽  
Jacqueline M. Burrows ◽  
Denis J. Moss ◽  
Michelle Catalina ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Virus Infection ◽  
Cytotoxic T Lymphocytes ◽  
Epstein Barr Virus ◽  
Epstein Barr Virus Infection ◽  
Longitudinal Dynamics ◽  
Barr Virus ◽  
Epstein Barr ◽  
Barr Virus Infection

Abstract 470: Epstein-Barr virus-encoded miR-BART5 modulates PIAS3-pSTAT3 and p21waf1in gastric carcinoma cells

2017 ◽  
Author(s):  
Dong Ha Kim ◽  
Chan Jin Yoon ◽  
Jin-Seoub Kim ◽  
Sunyoung Park ◽  
Euno Choi ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epstein Barr Virus ◽  
Carcinoma Cells ◽  
Barr Virus ◽  
Epstein Barr
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