ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Induction of Systemic Autoimmunity by a Xenobiotic Requires Endosomal TLR Trafficking and Signaling from the Late Endosome and Endolysosome but Not Type I IFN.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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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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.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Endosome traffic in rheumatic diseases: mechanistic insights and therapeutic opportunities.Nature reviews. Rheumatology · 2026Review
- Discovery of Blood-Based Proteins That Mark Benzo[a]pyrene Modulation of Autoimmunity.International journal of molecular sciences · 2025Article
- Effect of Age on Xenobiotic-Induced Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Mercury poisoning-associated membranous nephropathy and autoimmune encephalitis.BMC nephrology · 2025Article
- The TLR7/9 adaptors TASL and TASL2 mediate IRF5-dependent antiviral responses and autoimmunity in mouse.Nature communications · 2025Article
- Endosomal traffic disorders: a driving force behind neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- Environment and systemic autoimmune rheumatic diseases: an overview and future directions.Frontiers in immunology · 2024Review
- Article
- Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020Review
- Mercury-induced inflammation and autoimmunity.Biochimica et biophysica acta. General subjects · 2019Review
- Cross-Disease Innate Gene Signature: Emerging Diversity and Abundance in RA Comparing to SLE and SSc.Journal of immunology research · 2019Article
- Environmental Exposures and Autoimmune Diseases: Contribution of Gut Microbiome.Frontiers in immunology · 2019Review
- Environmental Xenobiotic Exposure and Autoimmunity.Current opinion in toxicology · 2018Article
- TLR7-Mediated Lupus Nephritis Is Independent of Type I IFN Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Type I IFN and nucleic acid-sensing TLRs are both strongly implicated in the pathogenesis of lupus, with most patients expressing IFN-induced genes in peripheral blood cells and with TLRs promoting type I IFNs and autoreactive B cells. About a third of systemic lupus erythematosus patients, however, lack the IFN signature, suggesting the possibility of type I IFN-independent mechanisms. In this study, we examined the role of type I IFN and TLR trafficking and signaling in xenobiotic systemic mercury-induced autoimmunity (HgIA). Strikingly, autoantibody production in HgIA was not dependent on the type I IFN receptor even in NZB mice that require type I IFN signaling for spontaneous disease, but was dependent on the endosomal TLR transporter UNC93B1 and the endosomal proton transporter, solute carrier family 15, member 4. HgIA also required the adaptor protein-3 complex, which transports TLRs from the early endosome to the late endolysosomal compartments. Examination of TLR signaling pathways implicated the canonical NF-κB pathway and the proinflammatory cytokine IL-6 in autoantibody production, but not IFN regulatory factor 7. These findings identify HgIA as a novel type I IFN-independent model of systemic autoimmunity and implicate TLR-mediated NF-κB proinflammatory signaling from the late endocytic pathway compartments in autoantibody generation.
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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.