例如："lncRNA", "apoptosis", "WRKY"

Epstein-Barr virus peptides derived from latent cycle proteins alter NKG2A + NK cell effector function.

Sci Rep. 2020 Nov 17;10(1):19973
Berenice Mbiribindi 1 , Josselyn K Pena 1 , Matthew P Arvedson 1 , Claudia Moreno Romero 1 , Sarah R McCarthy 1 , Olivia L Hatton 2 , Carlos O Esquivel 1 , Olivia M Martinez 1 , Sheri M Krams 3
Berenice Mbiribindi 1 , Josselyn K Pena 1 , Matthew P Arvedson 1 , Claudia Moreno Romero 1 , Sarah R McCarthy 1 , Olivia L Hatton 2 , Carlos O Esquivel 1 , Olivia M Martinez 1 , Sheri M Krams 3
+ et al

[No authors listed]

Author information
  • 1 Division of Abdominal Transplantation, Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • 2 Department of Molecular Biology, Colorado College, Colorado Springs, CO, USA.
  • 3 Division of Abdominal Transplantation, Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA. smkrams@stanford.edu.

摘要

Natural killer (NK) cells control viral infection through the interaction between inhibitory receptors and human leukocyte antigen (HLA) ligands and bound peptide. NK cells expressing the inhibitory receptor NKG2A/CD94 recognize and respond to autologous B cells latently infected with Epstein-Barr virus (EBV). The mechanism is not yet understood, thus we investigated peptides derived from seven latent proteins of EBV in the interaction of NKG2A and its ligand HLA-E. Functional analysis demonstrated that EBV peptides can bind to HLA-E and block inhibition of NK cell effector function. Moreover, analysis of DNA from 79 subjects showed sequence variations in the latent protein, LMP1, which alters NK responses to EBV. We provide evidence that peptides derived from EBV latent cycle proteins can impair the recognition of NKG2A despite being presented by HLA-E, resulting in NK cell activation.

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