ArticleCell reports methods2026
Induced pluripotent stem cell-derived macrophages enable broad modeling of human inflammasome signaling.
Article in Cell reports methods, 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.
- Protocol to study inflammasome activation in induced pluripotent stem cell-derived macrophages.STAR protocols · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage models are a mainstay of inflammasome research; however, current in vitro models have significant limitations. Here, we generate induced pluripotent stem cell (iPSC)-derived macrophages (iMacs) to study inflammasome signaling and benchmark them with human monocyte-derived macrophages. We confirm that iMacs express high levels of macrophage markers and are highly phagocytic. Proteomic analysis shows iMacs express many inflammasome sensors and related proteins, and iMacs respond to multiple inflammasome stimuli. The NLRP3 inflammasome is strongly activated in iMacs, and nigericin alone activates NLRP3. The non-canonical inflammasome does not require a priming step, and high NAIP/NLRC4 activation is observed in response to needle toxin. Finally, unlike human monocyte-derived macrophages (HMDMs), talabostat activates NLRP1 in iMacs. Therefore, we demonstrate that iMacs are a physiologically relevant and attractive model to study inflammasome signaling.
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.