ReviewCommunications biology2026
Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis.
Review in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Inflammasome-derived biomarkers in wound healing: linking tissue repair, chronic inflammation, fibrosis, and precision therapeutics.Molecular biology reports · 2026Review
- Autoinflammation with infantile enterocolitis associated with a novel CARD domain mutation inFrontiers in pediatrics · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRC4 inflammasome is a cytosolic immune sensor that detects bacterial virulence structures and rapidly initiates inflammatory responses. While tightly regulated NLRC4 activation is essential for host defense, genetic mutations that enhance NLRC4 signaling can drive severe autoinflammatory disease. Studies in patients and genetically engineered mouse models have begun to reveal how dysregulated NLRC4 activation disrupts intestinal and systemic immune homeostasis. This review summarizes current insights into NLRC4-associated autoinflammatory diseases, with particular emphasis on the mechanisms underlying autoinflammation with infantile enterocolitis, and highlights emerging concepts related to disease heterogeneity and therapeutic targeting.
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Registered trials
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