ArticleThe Journal of experimental medicine2005
Toll-like receptor 9 controls anti-DNA autoantibody production in murine lupus.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 2 of them syntheses that pooled it.
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
236 citing papers in PubMed, 2 syntheses or guidelines pooled it, 510 citations in OpenAlex.
- Emerging trends and focus of Toll-like receptors in kidney diseases: a 20-year bibliometric analysis.Frontiers in medicine · 2025Pooled it
- TLR9 polymorphisms and systemic lupus erythematosus risk: an update meta-analysis study.Rheumatology international · 2016Pooled it
- Association of the polymorphism of the Toll-like receptor (TLR)-3 and TLR-9 genes with hepatitis C virus-specific cell-mediated immunity outcomes among Egyptian health-care workers.Clinical and experimental immunology · 2021Trial
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- The transcription factor EHF promotes the maturation and immunosuppression of conventional dendritic cells.Nature communications · 2026Article
- The landscape of cellular immune alteration in systemic lupus erythematosus.Frontiers in immunology · 2026Review
- TLR7 and TLR9 have overlapping but distinct roles in systemic lupus erythematosus and Sjögren's disease.Frontiers in immunology · 2026Review
- S-TIR-ring up TLR7 and TLR9: signaling domain substitutions clarify the TLR paradox.The Journal of clinical investigation · 2025Article
- Knowledge mapping of plasmacytoid dendritic cells in systemic lupus erythematosus: a bibliometric analysis (2004-2023).Clinical rheumatology · 2025Article
- Review
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Innate Immune Receptors as Dynamic Modulators of Extrafollicular Autoimmune B Cell Response.Immunological reviews · 2025Review
- TLR9: A Double-Dealing Toll-Like Receptor.ImmunoTargets and therapy · 2025Review
- Review
- Systemic lupus erythematosus: pathogenesis and targeted therapy.Molecular biomedicine · 2024Review
- Directing risky traffic in B cells with TNIP1.Nature immunology · 2024Article
- Bank1 modulates the differentiation and molecular profile of key B cell populations in autoimmunity.JCI insight · 2024Article
- Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- Failed Downregulation of PI3K Signaling Makes Autoreactive B Cells Receptive to Bystander T Cell Help.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Toll-like receptor 9 (TLR9) genetic variants rs187084 and rs352140 confer protection from Behcet's disease among Iranians.BMC rheumatology · 2024Article
176 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
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Systemic autoimmune disease in humans and mice is characterized by loss of immunologic tolerance to a restricted set of self-nuclear antigens. Autoantigens, such as double-stranded (ds) DNA and the RNA-containing Smith antigen (Sm), may be selectively targeted in systemic lupus erythematosus because of their ability to activate a putative common receptor. Toll-like receptor 9 (TLR9), a receptor for CpG DNA, has been implicated in the activation of autoreactive B cells in vitro, but its role in promoting autoantibody production and disease in vivo has not been determined. We show that in TLR9-deficient lupus-prone mice, the generation of anti-dsDNA and antichromatin autoantibodies is specifically inhibited. Other autoantibodies, such as anti-Sm, are maintained and even increased in TLR9-deficient mice. In contrast, ablation of TLR3, a receptor for dsRNA, did not inhibit the formation of autoantibodies to either RNA- or DNA-containing antigens. Surprisingly, we found that despite the lack of anti-dsDNA autoantibodies in TLR9-deficient mice, there was no effect on the development of clinical autoimmune disease or nephritis. These results demonstrate a specific requirement for TLR9 in autoantibody formation in vivo and indicate a critical role for innate immune activation in autoimmunity.
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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.