Role of latent membrane protein 1 in chronic active Epstein–Barr virus infection‐derived T/NK‐cell proliferation. (3rd May 2014)

• Record Type: Journal Article
• Authors: Ito, Takuto; Kawazu, Hidetaka; Murata, Takayuki; Iwata, Seiko; Arakawa, Saki; Sato, Yoshitaka; Kuzushima, Kiyotaka; Goshima, Fumi; Kimura, Hiroshi
• Is Part Of: Cancer medicine. Volume 3:Number 4(2014:Aug.)
• Page Start: 787
• Page End: 795
• Publication Date: 2014-05-03
• Subjects: 616.994005
• DOI: 10.1002/cam4.256
• Languages: English
• ISSNs: 2045-7634

Abstract

<abstract abstract-type="main" id="cam4256-abs-0001"> <title>Abstract</title> <p>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 (LMP1) 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 LMP1 on EBV‐negative cells using the cells conditionally expressing LMP1, and on CAEBV‐derived EBV‐positive cells by inhibiting the function of LMP1 using a dominant negative form of LMP1. We demonstrated that LMP1 was responsible for the increased cell proliferation in the cell lines derived from CAEBV, while LMP1 did not give any proliferative advantage to the EBV‐negative cell line.</p> </abstract>