ArticlePloS one2012
Treatment of autoimmune inflammation by a TLR7 ligand regulating the innate immune system.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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
11 citing papers in PubMed, 25 citations in OpenAlex.
- Sex-Related Differences in Circular RNA Expression in Multiple Sclerosis: A Pilot Study.Journal of molecular neuroscience : MN · 2026Article
- Systemic microbial antigen administration ameliorates experimental autoimmune encephalomyelitis via MHC-II downregulation in the CNS and secondary lymphoid organs.Journal of neuropathology and experimental neurology · 2026Article
- Microbiome-Induced Autoimmunity and Novel Therapeutic Intervention.Advances in experimental medicine and biology · 2023Review
- Innate Signaling in the CNS Prevents Demyelination in a Focal EAE Model.Frontiers in neuroscience · 2021Article
- Revisiting the Hygiene Hypothesis in the Context of Autoimmunity.Frontiers in immunology · 2020Review
- Recent Advances and Perspectives in Small-molecule TLR Ligands and Their Modulators.ACS medicinal chemistry letters · 2018Article
- The hygiene hypothesis in autoimmunity: the role of pathogens and commensals.Nature reviews. Immunology · 2018Review
- TLR7 Signaling Regulates Th17 Cells and Autoimmunity: Novel Potential for Autoimmune Therapy.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Induction of Tolerogenic Dendritic Cells by a PEGylated TLR7 Ligand for Treatment of Type 1 Diabetes.PloS one · 2015Article
- Innate immune responses in the CNS: role of toll-like receptors, mechanisms, and therapeutic opportunities in multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The Toll-like receptors (TLR) have been advocated as attractive therapeutic targets because TLR signaling plays dual roles in initiating adaptive immune responses and perpetuating inflammation. Paradoxically, repeated stimulation of bone marrow mononuclear cells with a synthetic TLR7 ligand 9-benzyl-8-hydroxy-2-(2-methoxyethoxy) adenine (called 1V136) leads to subsequent TLR hyporesponsiveness. Further studies on the mechanism of action of this pharmacologic agent demonstrated that the TLR7 ligand treatment depressed dendritic cell activation, but did not directly affect T cell function. To verify this mechanism, we utilized experimental allergic encephalitis (EAE) as an in vivo T cell dependent autoimmune model. Drug treated SJL/J mice immunized with proteolipid protein (PLP)(139-151) peptide had attenuated disease severity, reduced accumulation of mononuclear cells in the central nervous system (CNS), and limited demyelination, without any apparent systemic toxicity. Splenic T cells from treated mice produced less cytokines upon antigenic rechallenge. In the spinal cords of 1V136-treated EAE mice, the expression of chemoattractants was also reduced, suggesting innate immune cell hyposensitization in the CNS. Indeed, systemic 1V136 did penetrate the CNS. These experiments indicated that repeated doses of a TLR7 ligand may desensitize dendritic cells in lymphoid organs, leading to diminished T cell responses. This treatment strategy might be a new modality to treat T cell mediated autoimmune diseases.
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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.