ArticleNature communications2026
Histone deacetylase inhibition induces an antitumor IRF8-dependent trained immunity-like status in macrophages.
Article in Nature communications, 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
11 authors.
Funding
Abstract
Epigenetic reprogramming underlies innate immune memory. However, whether trained immunity can be induced via epigenetic intervention to combat tumors, and the key regulators controlling this process, remain unclear. Here, we demonstrate that histone deacetylase inhibitor (HDACi) priming establishes a trained immunity-like state in monocytes/macrophages, conferring potent antitumor effect in multiple models of triple-negative breast cancer (TNBC) in female mice. Interferon regulatory factor 8 (IRF8) is identified as the master regulator of the inflammatory transcriptional program, which is governed by IRF8-associated super-enhancers and reinforced by HDACi. Myeloid-specific IRF8 deficiency impairs pro-inflammatory macrophage differentiation and abrogates HDACi-induced antitumor efficacy. Moreover, an IRF8-driven, CCL8-expressing macrophage subset recruits and activates cytotoxic CCR5
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.