ArticleToxicological sciences : an official journal of the Society of Toxicology2016
Immunomodulation By Subchronic Low Dose 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in Experimental Autoimmune Encephalomyelitis in the Absence of Pertussis Toxin.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 25 citations in OpenAlex.
- Using the Key Characteristics Framework to Unlock the Mysteries of Aryl Hydrocarbon Receptor-Mediated Effects on the Immune System.Annual review of immunology · 2025Review
- Modulation of Ceramide-Induced Apoptosis in Enteric Neurons by Aryl Hydrocarbon Receptor Signaling: Unveiling a New Pathway beyond ER Stress.International journal of molecular sciences · 2024Article
- Oxytocin and Vasopressin Gene Expression in the Brain as Potential Biomarkers for Cannabidiol Therapeutic Efficacy.Biomedicines · 2024Article
- Article
- Potential for TCDD to induce regulatory functions in B cells as part of the mechanism for T cell suppression in EAE.Toxicology and applied pharmacology · 2022Article
- TCDD Inhibition of IgG1 Production in Experimental Autoimmune Encephalomyelitis (EAE) and In Vitro.Antibodies (Basel, Switzerland) · 2022Article
- Isolation of Transcriptomic-Quality Total RNA from Mouse Spinal Cords.Current protocols · 2022Article
- Prophylactic and Therapeutic Effect of Kynurenine for Experimental Autoimmune Encephalomyelitis (EAE) Disease.International journal of tryptophan research : IJTR · 2022Article
- Targeting AhR as a Novel Therapeutic Modality against Inflammatory Diseases.International journal of molecular sciences · 2021Review
- TCDD attenuates EAE through induction of FasL on B cells and inhibition of IgG production.Toxicology · 2021Article
- Neuroinflammation and B-Cell Phenotypes in Cervical and Lumbosacral Regions of the Spinal Cord in Experimental Autoimmune Encephalomyelitis in the Absence of Pertussis Toxin.Neuroimmunomodulation · 2019Article
- The Aryl Hydrocarbon Receptor and the Nervous System.International journal of molecular sciences · 2018Review
- Role of AhR in positive regulation of cell proliferation and survival.Cell proliferation · 2016Review
- Divergent Ah Receptor Ligand Selectivity during Hominin Evolution.Molecular biology and evolution · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an autoimmune neurodegenerative disorder, characterized by demyelination of neurons in the central nervous system. To investigate the pathogenicity of various T cell types in MS, especially IFN-γ- or IL-17-producing CD4(+ )cells (TH1 or TH17 cells, respectively), the mouse model, experimental autoimmune encephalomyelitis (EAE), is commonly used. One method by which EAE is induced is immunization with myelin oligodendrocyte glycoprotein (MOG) peptide (MOG35-55) followed by subsequent injections of pertussis toxin (PTX) as an adjuvant. We have an interest in the mechanisms by which EAE occurs in the absence of PTX because it induces a milder disease state more consistent with autoimmune disease onset and PTX inactivates Gi/o protein-coupled receptors, many of which contribute to immune homeostasis. Another receptor that plays a role in immune homeostasis is the aryl hydrocarbon receptor (AHR). In fact, the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to attenuate EAE pathogenesis by affecting CD4(+ )T and regulatory T (Treg) cells in an AHR-dependent manner. However, many of these studies have been conducted with an acute high dose TCDD. Thus, the goal of this work was to investigate the modulation of MOG-specific immune responses with subchronic low dose TCDD (0.1-1.0 μg/kg/d for 12 days) in EAE without PTX. The results demonstrate that subchronic, low dose exposure of TCDD attenuates the immune responses in EAE development in the absence of PTX, which is due in part to suppression of MOG-specific IL-17A and IFN-γ responses.
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