ArticleThe Journal of experimental medicine2021
Viral infection modulates Qa-1b in infected and bystander cells to properly direct NK cell killing.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Single-Cell Transcriptome Profiling Reveals the Immune Dysregulation Characteristics of Mice Infected With Brucella abortus.The Journal of infectious diseases · 2026Article
- Innate and adaptive immune responses that control lymph-borne viruses in the draining lymph node.Cellular & molecular immunology · 2024Review
- IFN-γ in ovarian tumor microenvironment upregulates HLA-E expression and predicts a poor prognosis.Journal of ovarian research · 2023Article
- Resistance To Poxvirus Lethality Does Not Require the Necroptosis Proteins RIPK3 or MLKL.Journal of virology · 2023Article
- NK cell subsets and dysfunction during viral infection: a new avenue for therapeutics?Frontiers in immunology · 2023Review
- Interferon partly dictates a divergent transcriptional response in poxvirus-infected and bystander inflammatory monocytes.Cell reports · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Natural killer (NK) cell activation depends on the signaling balance of activating and inhibitory receptors. CD94 forms inhibitory receptors with NKG2A and activating receptors with NKG2E or NKG2C. We previously demonstrated that CD94-NKG2 on NK cells and its ligand Qa-1b are important for the resistance of C57BL/6 mice to lethal ectromelia virus (ECTV) infection. We now show that NKG2C or NKG2E deficiency does not increase susceptibility to lethal ECTV infection, but overexpression of Qa-1b in infected cells does. We also demonstrate that Qa-1b is down-regulated in infected and up-regulated in bystander inflammatory monocytes and B cells. Moreover, NK cells activated by ECTV infection kill Qa-1b-deficient cells in vitro and in vivo. Thus, during viral infection, recognition of Qa-1b by activating CD94/NKG2 receptors is not critical. Instead, the levels of Qa-1b expression are down-regulated in infected cells but increased in some bystander immune cells to respectively promote or inhibit their killing by activated NK cells.
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Registered trials
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