AI reveals gene defect driving Crohn’s disease
Molecular biology and AI have solved a decades-old mystery, paving the way for targeted Crohn’s disease treatments.
Scientists at UC San Diego used AI and molecular biology to show how a broken NOD2–girdin partnership causes chronic inflammation in Crohn’s disease. The study explains why some macrophages become inflammatory instead of restorative, leading to intestinal damage.
The study analysed thousands of macrophage genes, identifying 53 that separate inflammatory cells from healing ones. One key discovery revealed that NOD2 normally binds to girdin in non-inflammatory macrophages, keeping inflammation under control.
Mutations in NOD2, common in Crohn’s patients, disrupt this connection, tipping the immune system toward persistent gut inflammation.
Animal studies confirmed the findings. Mice lacking girdin developed severe intestinal inflammation, altered gut microbiomes, and in many cases, fatal sepsis.
The experiments showed that without the NOD2–girdin interaction, the gut’s immune balance collapses, highlighting the importance of this partnership for intestinal health.
By combining AI, genetic analysis, and animal models, the study opens new avenues for Crohn’s therapies. Researchers aim to restore the NOD2–girdin interaction to rebalance macrophages and ease chronic inflammation.
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