ArticleNature immunology2018
Selective autophagy of the adaptor TRIF regulates innate inflammatory signaling.
Article in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed, 129 citations in OpenAlex.
- Type I interferon signaling promotes mucosal inflammation in murine models of colitis.bioRxiv : the preprint server for biology · 2026Article
- Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026Review
- Negative feedback regulation of STING signaling by TAX1BP1-directed Golgiphagy.Nature communications · 2026Article
- Cell death and immune escape in the tumor microenvironment: associated mechanisms, opportunities and challenges.Apoptosis : an international journal on programmed cell death · 2026Review
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Emerging Nanomedicine Strategies for Sepsis: Immunomodulation and Beyond.Research (Washington, D.C.) · 2026Article
- Roles of Deubiquitinases OTUD3 and OTUD5 in Inflammatory Bowel Diseases.International journal of molecular sciences · 2025Review
- Salmonella typhimurium downregulates circHIPK2 expression via CeRNA mechanism to inhibit cell migration and tumorigenesis.Gut pathogens · 2025Article
- Pattern recognition receptors and inflammasome: Now and beyond.Molecules and cells · 2025Review
- Article
- Article
- Article
- Exploration potential sepsis-ferroptosis mechanisms through the use of CETSA technology and network pharmacology.Scientific reports · 2025Article
- Autophagy in Tissue Repair and Regeneration.Cells · 2025Review
- RNF128 deficiency in macrophages promotes colonic inflammation by suppressing the autophagic degradation of S100A8.Cell death & disease · 2025Article
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Article
- The preventive and therapeutic role of Lactobacillus spp. in in vitro model of inflammation via affecting autophagy signaling pathway.Immunity, inflammation and disease · 2024Article
- Osteogenesis imperfecta type 10 and the cellular scaffolds underlying common immunological diseases.Genes and immunity · 2024Review
- Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defective autophagy is linked to diseases such as rheumatoid arthritis, lupus and inflammatory bowel disease (IBD). However, the mechanisms by which autophagy limits inflammation remain poorly understood. Here we found that loss of the autophagy-related gene Atg16l1 promoted accumulation of the adaptor TRIF and downstream signaling in macrophages. Multiplex proteomic profiling identified SQSTM1 and Tax1BP1 as selective autophagy-related receptors that mediated the turnover of TRIF. Knockdown of Tax1bp1 increased production of the cytokines IFN-β and IL-1β. Mice lacking Atg16l1 in myeloid cells succumbed to lipopolysaccharide-mediated sepsis but enhanced their clearance of intestinal Salmonella typhimurium in an interferon receptor-dependent manner. Human macrophages with the Crohn's disease-associated Atg16l1 variant T300A exhibited more production of IFN-β and IL-1β. An elevated interferon-response gene signature was observed in patients with IBD who were resistant to treatment with an antibody to the cytokine TNF. These findings identify selective autophagy as a key regulator of signaling via the innate immune system.
Indexed as
Identifiers
What OpenQuestion holds
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.