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• W2096003818 abstract "The Epstein-Barr virus (EBV) nuclear antigen (EBNA)1 contains a glycine-alanine repeat (GAr) domain that appears to protect the antigen from proteasomal breakdown and, as measured in cytotoxicity assays, from major histocompatibility complex (MHC) class I–restricted presentation to CD8+ T cells. This led to the concept of EBNA1 as an immunologically silent protein that although unique in being expressed in all EBV malignancies, could not be exploited as a CD8 target. Here, using CD8+ T cell clones to native EBNA1 epitopes upstream and downstream of the GAr domain and assaying recognition by interferon γ release, we show that the EBNA1 naturally expressed in EBV-transformed lymphoblastoid cell lines (LCLs) is in fact presented to CD8+ T cells via a proteasome/peptide transporter–dependent pathway. Furthermore, LCL recognition by such CD8+ T cells, although slightly lower than seen with paired lines expressing a GAr-deleted EBNA1 protein, leads to strong and specific inhibition of LCL outgrowth in vitro. Endogenously expressed EBNA1 is therefore accessible to the MHC class I pathway despite GAr-mediated stabilization of the mature protein. We infer that EBNA1-specific CD8+ T cells do play a role in control of EBV infection in vivo and might be exploitable in the control of EBV+ malignancies." @default.
• W2096003818 created "2016-06-24" @default.
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• W2096003818 date "2004-05-17" @default.
• W2096003818 modified "2023-10-06" @default.
• W2096003818 title "CD8 T Cell Recognition of Endogenously Expressed Epstein-Barr Virus Nuclear Antigen 1" @default.
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• W2096003818 doi "https://doi.org/10.1084/jem.20040121" @default.
• W2096003818 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2211813" @default.
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