ArticlePloS one2011
Activation of the alternative NFκB pathway improves disease symptoms in a model of Sjogren's syndrome.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Ameliorating Active Ulcerative Colitis via an Orally Available Toll-Like Receptor-9 Modifier: A Prospective Open-Label, Multicenter Phase II Trial.Digestive diseases and sciences · 2016Trial
- Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026Review
- The causal relationship between immune cells and Sjögren's syndrome: a univariate, multivariate, bidirectional Mendelian randomized study.Frontiers in medicine · 2024Article
- Cell-Free DNA in the Pathogenesis and Therapy of Non-Infectious Inflammations and Tumors.Biomedicines · 2022Review
- Nucleic acid-sensing toll-like receptors: Important players in Sjögren's syndrome.Frontiers in immunology · 2022Review
- CpG-ODN-mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression.Immunology · 2020Article
- Emerging Mechanisms of Innate Immunity and Their Translational Potential in Inflammatory Bowel Disease.Frontiers in medicine · 2018Review
- Current and Emerging Evidence for Toll-Like Receptor Activation in Sjögren's Syndrome.Journal of immunology research · 2018Review
- Review on Toll-Like Receptor Activation in Myasthenia Gravis: Application to the Development of New Experimental Models.Clinical reviews in allergy & immunology · 2017Review
- Recent Advances in Aptamers Targeting Immune System.Inflammation · 2017Review
- Downstream activation of NF-κB in the EDA-A1/EDAR signalling in Sjögren's syndrome and its regulation by the ubiquitin-editing enzyme A20.Clinical and experimental immunology · 2016Article
- Desiccating stress-induced disruption of ocular surface immune tolerance drives dry eye disease.Clinical and experimental immunology · 2016Article
- Gut feeling: MicroRNA discriminators of the intestinal TLR9-cholinergic links.International immunopharmacology · 2015Article
- The clinical relevance of animal models in Sjögren's syndrome: the interferon signature from mouse to man.Arthritis research & therapy · 2015Review
- Role of α7 nicotinic receptor in the immune system and intracellular signaling pathways.Central-European journal of immunology · 2015Review
- Antibody- and aptamer-strategies for GvHD prevention.Journal of cellular and molecular medicine · 2015Review
- Rituximab-mediated Raf kinase inhibitor protein induction modulates NF-κB in Sjögren syndrome.Immunology · 2014Article
- Epistasis with HLA DR3 implicates the P2X7 receptor in the pathogenesis of primary Sjögren's syndrome.Arthritis research & therapy · 2013Article
- Presymptomatic treatment with acetylcholinesterase antisense oligonucleotides prolongs survival in ALS (G93A-SOD1) mice.BioMed research international · 2013Article
- Stressing hematopoiesis and immunity: an acetylcholinesterase window into nervous and immune system interactions.Frontiers in molecular neuroscience · 2012Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of our study was to understand if Toll-like receptor 9 (TLR9) activation could contribute to the control of inflammation in Sjogren's syndrome. To this end, we manipulated TLR9 signaling in non-obese diabetic (NOD) and TLR9(-/-) mice using agonistic CpG oligonucleotide aptamers, TLR9 inhibitors, and the in-house oligonucleotide BL-7040. We then measured salivation, inflammatory response markers, and expression of proteins downstream to NF-κB activation pathways. Finally, we labeled proteins of interest in salivary gland biopsies from Sjogren's syndrome patients, compared to Sicca syndrome controls. We show that in NOD mice BL-7040 activates TLR9 to induce an alternative NF-κB activation mode resulting in increased salivation, elevated anti-inflammatory response in salivary glands, and reduced peripheral AChE activity. These effects were more prominent and also suppressible by TLR9 inhibitors in NOD mice, but TLR9(-/-) mice were resistant to the salivation-promoting effects of CpG oligonucleotides and BL-7040. Last, salivary glands from Sjogren's disease patients showed increased inflammatory and decreased anti-inflammatory biomarkers, in addition to decreased levels of alternative NF-κB pathway proteins. In summary, we have demonstrated that activation of TLR9 by BL-7040 leads to non-canonical activation of NF-κB, promoting salivary functioning and down-regulating inflammation. We propose that BL-7040 could be beneficial in treating Sjogren's syndrome and may be applicable to additional autoimmune syndromes.
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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.