ArticleFrontiers in cellular and infection microbiology2026
An
Article in Frontiers in cellular and infection microbiology, 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.
- EZH1/2 inhibition improves immunotherapy response through MHC Class II de-repression and neutrophil reprogramming.bioRxiv : the preprint server for biology · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Chimeric antigen receptor (CAR) T-cell therapy has demonstrated remarkable efficacy in hematological malignancies. However, it can also cause severe systemic toxicity, known as cytokine release syndrome (CRS). Therefore, the potential of CAR-T cells to cause toxicity Methods: CAR-T cells, macrophages, or immature dendritic cells (iDCs), along with tumor target cells, were co-cultured under different conditions. The release of CRS-related cytokines, IFN-γ and IL-6, was measured to simulate cytokine release during CAR-T-induced CRS. Additionally, the cellular source of the key CRS cytokine IL-6 was investigated. Results: A co-culture system containing only CAR-T cells and tumor cells failed to recapitulate the key feature of CRS, specifically a significant elevation of IL-6. However, when CAR-T cells were co-cultured with antigen-presenting cells (macrophages or iDCs) and tumor cells, the core CRS cytokine IL-6 was significantly elevated in an Conclusion: Macrophages and iDCs play a critical role in the development of CAR-T therapy-induced CRS. The triple-cell co-culture system, comprising CAR-T cells, macrophages or iDCs, and tumor cells, provides a viable
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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.