Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis

Yuhang Wang; Sivakumar Lingappa; Zizhen Kang

doi:10.1038/s42003-026-10174-3

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Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis

Journal article

Open access

Peer reviewed

Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis

Yuhang Wang, Sivakumar Lingappa and Zizhen Kang

Communications biology, Vol.9(1), 611

05/05/2026

DOI: 10.1038/s42003-026-10174-3

PMID: 42082718

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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.

Animals

Apoptosis Regulatory Proteins - genetics

Apoptosis Regulatory Proteins - metabolism

Calcium-Binding Proteins - genetics

Calcium-Binding Proteins - immunology

Calcium-Binding Proteins - metabolism

CARD Signaling Adaptor Proteins - genetics

CARD Signaling Adaptor Proteins - metabolism

Enterocolitis - genetics

Enterocolitis - immunology

Enterocolitis - metabolism

Humans

Inflammasomes - genetics

Inflammasomes - immunology

Inflammasomes - metabolism

Inflammation - immunology

Mice

Details

Title: Subtitle: Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis
Creators: Yuhang Wang - University of Iowa
Sivakumar Lingappa - University of Iowa
Zizhen Kang - University of Iowa
Resource Type: Journal article
Publication Details: Communications biology, Vol.9(1), 611
DOI: 10.1038/s42003-026-10174-3
PMID: 42082718
ISSN: 2399-3642
eISSN: 2399-3642
Publisher: NATURE PORTFOLIO
Grant note: University of Iowa (UI) This work was supported by startup funding provided by the Department of Pathology, Carver College of Medicine, University of Iowa.
The authors apologize to colleagues whose important contributions could not be cited due to space limitations and acknowledge the many investigators whose work has advanced the field. This work was supported by startup funding provided by the Department of Pathology, Carver College of Medicine, University of Iowa.
Language: English
Date published: 05/05/2026
Academic Unit: Pathology; Iowa Neuroscience Institute; Periodontics
Record Identifier: 9985163399202771

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