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Targeting Epstein-Barr Virus–Associated Lymphomas

December 25, 2019


Targeting Epstein-Barr virus-associated
lymphomas. During stimulation of naive B cells by antigen, a progression from
activated B cell through the germinal center and differentiation to a memory
B cell occurs. After Epstein-Barr virus (EBV) infection of a naive B cell, different
programs of EBV-latent proteins are expressed that drive differentiation of
the infected B cell in an analogous manner. Viral expression of the full
panel of latent proteins– EBV nuclear antigen 1 (EBNA1) to EBNA6 and latent
membrane protein 1 (LMP1) and LMP2 in activated B cells, to EBNA1and LMP1
and LMP2 in germinal center cells, to EBNA1 alone in cycling memory B cells
recapitulate this same progression. Decrease in number and immunogenicity of EBV antigens enables viral persistence. EBV-specific cytotoxic T-cell lines (CTLs) were originally generated by exposure to EBV-transformed lymphoblastoid cell lines (EBV-LCLs) expressing Latency III. The resulting polyclonal cells are primarily directed
against the immunogenic EBNA3 proteins and recognize only malignancies
expressing Latency III such as post-transplantation lymphoproliferative
disorders (PTLDs) and immunoblastic lymphomas seen primarily in immunocompromised
individuals. Stimulation with dendritic cells transduced with an adenoviral
vector containing a truncated LMP1 and LMP2 construct before stimulation with
similarly transduced EBV-LCLs also yields CTLs with high reactivity to
LMP1 and LMP2. These CTLs are capable of recognizing malignancies expressing
Latency II such as Hodgkin lymphoma, diffuse large
B-cell lymphoma (DLBCL), and T-cell lymphomas seen in immunocompetent individuals.
These CTLs are not designed to recognize Burkitt’s lymphoma, which
expresses the Latency I program.

1 Comment

  • Reply RealEstateInsider247 August 19, 2019 at 4:05 am

    English please.

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