ArticleToxicological sciences : an official journal of the Society of Toxicology2017
From the Cover: Interplay Between IFN-γ and IL-6 Impacts the Inflammatory Response and Expression of Interferon-Regulated Genes in Environmental-Induced Autoimmunity.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2017. 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, 24 citations in OpenAlex.
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- Candidate approaches for predicting vitiligo recurrence: an effective model and biomarkers.Frontiers in immunology · 2025Article
- Alterations in Plasma Cytokine Levels in Korean Children with Autism Spectrum Disorder.Yonsei medical journal · 2024Article
- Systemic maternal inflammation promotes ASD via IL-6 and IFN-γ.Bioscience reports · 2022Review
- Which Therapy for Non-Type(T)2/T2-Low Asthma.Journal of personalized medicine · 2021Review
- Circulating mature granzyme B+ T cells distinguish Crohn's disease-associated axial spondyloarthritis from axial spondyloarthritis and Crohn's disease.Arthritis research & therapy · 2021Article
- Mechanisms of Environment-Induced Autoimmunity.Annual review of pharmacology and toxicology · 2021Article
- Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020Review
- Immune System Effects of Insulin-Like Peptide 5 in a Mouse Model.Frontiers in endocrinology · 2020Article
- Mercury-induced inflammation and autoimmunity.Biochimica et biophysica acta. General subjects · 2019Review
- Environmental Xenobiotic Exposure and Autoimmunity.Current opinion in toxicology · 2018Article
- Featured Article: Modulation of the OGF-OGFr pathway alters cytokine profiles in experimental autoimmune encephalomyelitis and multiple sclerosis.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Quantitative Proteomic Analysis Reveals That Arctigenin Alleviates Concanavalin A-Induced Hepatitis Through Suppressing Immune System and Regulating Autophagy.Frontiers in immunology · 2018Article
- Induction of Systemic Autoimmunity by a Xenobiotic Requires Endosomal TLR Trafficking and Signaling from the Late Endosome and Endolysosome but Not Type I IFN.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
IFN-γ has been found to be robustly important to disease pathogenesis in both idiopathic and induced models of murine lupus. In transgenic mice, over production of IFN-γ in the skin results in an inflammatory response and autoimmunity. This suggests that localized exposure to environmental factors that induce autoimmunity may be associated with expression of an IFN-γ-dependent inflammatory response. Using murine mercury-induced autoimmunity (mHgIA), the severity of inflammation and proinflammatory cytokine expression, including the cellular source of IFN-γ, were assessed at the site of subcutaneous exposure and in secondary lymphoid organs. Exposure induced a localized chronic inflammation comprising both innate and adaptive immune cells but only CD8+ T and NK cells were reduced in the absence of IFN-γ. IFN-γ+ cells began to appear as early as day 1 and comprised both resident (γδ T) and infiltrating cells (CD8+ T, NKT, CD11c+). The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA. None of these genes were essential for induction of inflammation, however IFN-γ and IL-6 were required for exacerbation of other proinflammatory cytokines. Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN. Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA. Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity.
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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.