
Role of latent membrane protein 1 in chronic active Epstein–Barr virus infection‐derived T/NK‐cell proliferation
Author(s) -
Ito Takuto,
Kawazu Hidetaka,
Murata Takayuki,
Iwata Seiko,
Arakawa Saki,
Sato Yoshitaka,
Kuzushima Kiyotaka,
Goshima Fumi,
Kimura Hiroshi
Publication year - 2014
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.256
Subject(s) - biology , lymphoma , virus , epstein–barr virus , immunology , cell , cell growth , cancer research , b cell , virology , antibody , genetics
Epstein–Barr virus ( EBV ) predominantly infects B cells and causes B‐cell lymphomas, such as Burkitt lymphoma and Hodgkin lymphoma. However, it also infects other types of cells, including T and natural killer ( NK ) cells, and causes disorders, such as chronic active EBV infection ( CAEBV ) and T/ NK ‐cell lymphoma. The CAEBV is a lymphoproliferative disease with poor prognosis, where EBV ‐positive T or NK cells grow rapidly, although the molecular mechanisms that cause the cell expansion still remain to be elucidated. EBV ‐encoded latent membrane protein 1 ( LMP 1) is an oncogene that can transform some cell types, such as B cells and mouse fibroblasts, and thus may stimulate cell proliferation in CAEBV . Here, we examined the effect of LMP 1 on EBV ‐negative cells using the cells conditionally expressing LMP 1, and on CAEBV ‐derived EBV ‐positive cells by inhibiting the function of LMP 1 using a dominant negative form of LMP 1. We demonstrated that LMP 1 was responsible for the increased cell proliferation in the cell lines derived from CAEBV , while LMP 1 did not give any proliferative advantage to the EBV ‐negative cell line.