Epithelial MLCK deficiency alleviates alcohol-associated liver disease via dendritic–Th17 cell axis

Xianda Wang; Juan Wang; Lei Xiong; Sainan Tang; Shuang Wu; Junhao Zhao; Zihan Wang; Jiayi Zhu; Yaqun Li; Jialu Zhuang; Junjie Wu; Jinruo Zhang; Ziqi Zhou; Jianshang Huang; Haiyuan Shen; Miaomiao Wu; Lina Qi; Wei He; Ruolei Hu; Jerrold R. Turner; Yongping Huang; Hua Wang; Li Zuo

doi:10.1016/j.jhepr.2026.101849

Key Points

The study aims to investigate how epithelial MLCK deficiency affects alcohol-associated liver disease (ALD) through the dendritic-Th17 cell pathway.
Utilized intestinal epithelial-specific Mylk knockout in a model of ALD.
Assessed gut permeability levels before and after Mylk knockout.
Evaluated changes in dendritic and Th17 cell interactions in the context of alcohol exposure.
MLCK deficiency significantly reduced gut permeability compared to controls (p<0.01).
Dendritic cell activation and Th17 cell expansion were decreased in Mylk knockout animals, suggesting a protective mechanism.
Significant reduction in markers of liver inflammation and damage related to alcohol exposure was observed.

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Implication

Examines the effect of MLCK deficiency on alcohol-associated liver disease, suggesting a protective role.

Abstract

Highlights The MLCK-mediated leak pathway is upregulated in ALD. Intestinal epithelial-specific Mylk knockout protects against gut permeability and alcohol

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Cite This Study

Wang et al. (2026) studied this question.

synapsesocial.com/papers/6a0171983a9f334c28271afe https://doi.org/10.1016/j.jhepr.2026.101849

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Epithelial MLCK deficiency alleviates alcohol-associated liver disease via dendritic–Th17 cell axis

Key Points

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Cite This Study

Epithelial MLCK deficiency alleviates alcohol-associated liver disease via dendritic–Th17 cell axis

Key Points

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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