ArticleMolecular medicine (Cambridge, Mass.)2026
IL17F
Article in Molecular medicine (Cambridge, Mass.), 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.
- T-Cell Memory Affects Lung Responses to Cecal Ligation and Puncture.Shock (Augusta, Ga.) · 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
10 authors.
Funding
Abstract
T cell memory significantly alters the immune response and organ dysfunction induced by the murine cecal ligation and puncture (CLP) model of sepsis. Enhanced T cell memory activation promotes hepatic neutrophilic responses and induces hepatic dysfunction, which is a common complication of human sepsis associated with poor outcomes. We used a novel Immune Educated CLP sepsis mouse model to examine the role of memory T cell cytokine responses in driving innate immunity and organ dysfunction. Through this approach, we found that induced T cell memory prior to CLP led to higher serum levels of IL12, TNF, IL17, and IL1β – all dependent on memory CD8 T cell derived IFNγ following CLP. IFNγ induced activated hepatic IL12+ monocyte-derived dendritic cells. Increased neutrophilic responses occurred in Educated CLP which was found to depend on TNF, and were suppressed by IFNγ. Hepatic dysfunction in response to CLP was worsened by CD4 and CD8 T cell immune memory and prevented by IFNγ and IL17F blockade. These findings were recapitulated in naturalized outbred pet shop mice with natural immune memory to provide translational relevance to our Immune Educated CLP sepsis model. IL17F or IFNγ blockade may represent potential targets for treatment in sepsis with hepatic dysfunction.
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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.