Author:
Mbiribindi Berenice,Pena Josselyn K.,Arvedson Matthew P.,Moreno Romero Claudia,McCarthy Sarah R.,Hatton Olivia L.,Esquivel Carlos O.,Martinez Olivia M.,Krams Sheri M.
Abstract
AbstractNatural 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.
Funder
Transplant and Tissue Engineering Center of Excellence at Lucile Packard Children’s Hospital
the Stanford Maternal and Child Health Research Institute
NIH
Publisher
Springer Science and Business Media LLC
Cited by
19 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献