ArticleJournal of immunology (Baltimore, Md. : 1950)2026
NKG2A+ NK cell cytotoxicity of Epstein-Barr virus infected B cells is mediated through the NKG2D and NKp30 activating receptors.
Article in Journal of immunology (Baltimore, Md. : 1950), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Immunomodulatory Strategies for Managing Viral Infections in Solid Organ Transplantation: Progress and Challenges.Current microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Epstein-Barr virus (EBV) is a human γ-herpesvirus that establishes latency and lifelong infection in B cells. Failure to control latent EBV infection can result in a variety of malignancies, including lymphoproliferative diseases. Studies have implicated natural killer (NK) cells as critical in the host defense against lytic and latent EBV infection. To fully characterize NK cells that respond to latently infected cells, we generated a panel of EBV+ B lymphoblastoid cell lines (EBV+ LCL) and performed coculture experiments with autologous primary NK cells. EBV-responsive NK cells were analyzed for functional and phenotypic markers using mass cytometry. In addition to expression of the inhibitory NK cell receptor NKG2A, EBV-responsive NK cells express high levels of the NKp30 and NKG2D activating receptors which were shown to be important in mediating cytotoxicity of EBV+ LCL. NK cells from cohorts of EBV seropositive and EBV seronegative children were examined by mass cytometry for NK cell receptor expression and identified 4 NKG2A+ clusters, including the NKG2A+2B4+CD56+CD16-CD57-NKG2C-NKp30+NKG2D+ population. The importance of the NKG2A: HLA-E immune checkpoint axis was established using both HLA-E knockout EBV+ LCL and antibody blockade of NKG2A which demonstrated enhanced NK-mediated cytotoxicity in the absence of NKG2A-HLA-E interactions. Taken together, our results support that NKG2A+ NK cells are educated and functionally cytotoxic against EBV-infected B cells and suggest therapeutics targeting the NKG2A: HLA-E immune checkpoint axis would be a good option for EBV-associated malignancies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.