ArticlePloS one2026
Single-cell transcriptomic analysis reveals the immunosuppressive status of NK cell subpopulations in TNBC.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC), lacking expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), has clinical features that include high invasiveness, limited response to current immunotherapies, heightened risk of recurrence, and poorer overall prognosis. Central to these adverse clinical outcomes is the tumor microenvironment (TME), where the presence of immature natural killer (NK) cells with lower cytotoxic capacity has been associated with disease progression. Through a comprehensive analysis of publicly available single-cell transcriptomic data from breast cancer, we identified three NK cell subtypes within TNBC and non-TNBC tissues, named NK_XCL1, NK_FCGR3A, and NK_ISG15. Compared to non-TNBC, the presence and cytotoxic activity of NK_FCGR3A cells in TNBC were markedly diminished, primarily due to a substantial increase in the expression of inhibitory receptors like NKG2A (KLRC1). NK_ISG15 cells in TNBC show higher expression of type I interferon signaling genes. Through cell-type cross-talk analysis, we found that the feature of NK_FCGR3A cells in TNBC was mediated by myeloid cells with the HLA-E-KLRC1/HLA-E-CD94:NKG2A signal pathway. Notably, through integrating with public cancer transcriptomic data, we found higher expression of ISG15 is associated with poor prognosis, while higher expression of NK_FCGR3A signature genes is correlated with favorable prognosis. Collectively, these findings and the markers identified offer valuable insights into the mechanisms of immune evasion in TNBC, underscoring potential targets for developing therapeutic strategies that may improve patient outcomes.
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.