NK/T Lymphocytes and LMP1: An Update on the Interactions and Mechanisms of Regulation

Abstract

Epstein-Barr virus (EBV) is a strictly human virus of the family of Herpesviridae. It infects almost the entire population; the infection is often asymptomatic and benign. However, many studies show that this virus can also participate in the oncogenesis of various human malignancies of epithelial or lymphocytic origin. After the primary infection, EBV remains latent in the body. During this latency, some proteins are expressed, including LMP1 (latent membrane protein). This protein, located at the membrane level, induces several signalling pathways involved in the survival of the host cell. It is described as the major oncoprotein of EBV. EBV-encoded latent membrane protein 1 is a multifunctional oncoprotein essential for transforming B lymphocytes into lymphoblastoid cell lines. The LMP1 gene, also referred to as BNLF1, encoding the LMP1 protein is relatively well conserved in its coding region, generally showing greater than 95% amino acid sequence identity between the different EBV isolates. NK cells appear to play an important role in the early control of EBV infection in both mice and humans. Few studies were interested in the interaction between LMP1 and NK and T cells. The aim of this review is to collect articles discussing the interaction between LMP1 and NK and T cells in order to describe the mechanisms of control of LMP1 by the NK/T cells and how LMP1 can regulate and promote them.