ArticleEMBO reports2026
Preventing MALT1-mediated CYLD cleavage induces intestinal dysbiosis and reduces EAE severity.
Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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12 authors.
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Abstract
The paracaspase MALT1 is essential for lymphocyte activation and also plays roles in non-immune cells and cancer. Its protease activity regulates immune signaling by cleaving specific substrates, making it a promising therapeutic target. However, broad inhibition of MALT1 protease activity causes multiorgan inflammation in mice, highlighting the need to understand the effects of individual substrate cleavage. We generated CYLD(R321A) knock-in mice expressing a MALT1-resistant form of the deubiquitinase CYLD. These mice are healthy, with normal lymphocyte development and preserved immune signaling. Unlike MALT1 protease-dead mice, they do not develop spontaneous inflammation. Notably, they exhibit altered gut microbiota and reduced disease severity in a model of multiple sclerosis. Together, our work shows that blocking cleavage of a single MALT1 substrate is sufficient to modulate microbiota and neuroinflammation without causing overt defects in lymphocyte cell development or activation, providing in vivo evidence for substrate-specific targeting of MALT1 as a refined therapeutic strategy.
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