ArticleImmunity2025
Heterozygosity for Crohn's disease risk allele of ATG16L1 promotes unique protein interactions and protects against bacterial infection.
Article in Immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
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Who cites it
6 citing papers in PubMed.
- Canonical and noncanonical autophagy in immunity.Immunity · 2026Review
- Crohn's disease: research progress in decoding pathogenic multi-network and precision management of artificial intelligence radiomics.Frontiers in immunology · 2026Review
- SIRT2 Inhibition promotes microglia LC3-associated phagocytosis via NRF2/CD36 after the experimental subarachnoid hemorrhage.Journal of neuroinflammation · 2025Article
- Balancing immunity: disease risk mutation can be beneficial.Trends in immunology · 2025Article
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Anti-inflammatory effects of natural polysaccharides: molecular mechanisms and nanotherapeutic applications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The T300A substitution in ATG16L1 associated with Crohn's disease impairs autophagy, yet up to 50% of humans are heterozygous for this allele. Here, we demonstrate that heterozygosity for the analogous substitution in mice (Atg16L1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.