دورية أكاديمية

Mercury-induced inflammation and autoimmunity.

التفاصيل البيبلوغرافية
العنوان: Mercury-induced inflammation and autoimmunity.
المؤلفون: Pollard KM; Department of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America. Electronic address: mpollard@scripps.edu., Cauvi DM; Department of Surgery and Center for Investigations of Health and Education Disparities, School of Medicine, University of California, San Diego, 9500 Gilman Drive #0739, La Jolla, CA 92093, United States of America. Electronic address: dcauvi@ucsd.edu., Toomey CB; Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, CA 92093. Electronic address: cbtoomey@ucsd.edu., Hultman P; Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden. Electronic address: per.hultman@liu.se., Kono DH; Department of Immunology and Microbiology, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America. Electronic address: dkono@scripps.edu.
المصدر: Biochimica et biophysica acta. General subjects [Biochim Biophys Acta Gen Subj] 2019 Dec; Vol. 1863 (12), pp. 129299. Date of Electronic Publication: 2019 Feb 10.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101731726 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-8006 (Electronic) Linking ISSN: 03044165 NLM ISO Abbreviation: Biochim Biophys Acta Gen Subj Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam : Elsevier
مواضيع طبية MeSH: Autoimmune Diseases*/chemically induced , Autoimmune Diseases*/genetics , Autoimmune Diseases*/pathology , Gene Expression Regulation*/drug effects , Gene Expression Regulation*/immunology, Autoimmunity/*drug effects , Mercury/*toxicity, Animals ; Cytokines/genetics ; Cytokines/immunology ; Disease Models, Animal ; Genome-Wide Association Study ; Humans ; Inflammation/chemically induced ; Inflammation/immunology ; Inflammation/pathology
مستخلص: Background: Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.
Scope of the Review: In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.
Major Conclusions: Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.
General Significance: Mercury exposure likely contributes to the pathogenesis of autoimmunity.
(Copyright © 2019 Elsevier B.V. All rights reserved.)
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معلومات مُعتمدة: R01 ES022625 United States ES NIEHS NIH HHS; R21 ES029263 United States ES NIEHS NIH HHS; UH2 ES027679 United States ES NIEHS NIH HHS; UH3 ES027679 United States ES NIEHS NIH HHS; R01 ES021464 United States ES NIEHS NIH HHS
فهرسة مساهمة: Keywords: Animal model; Autoimmunity; Human; Inflammation; Mercury
المشرفين على المادة: 0 (Cytokines)
FXS1BY2PGL (Mercury)
تواريخ الأحداث: Date Created: 20190212 Date Completed: 20200512 Latest Revision: 20201201
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6689266
DOI: 10.1016/j.bbagen.2019.02.001
PMID: 30742953
قاعدة البيانات: MEDLINE
الوصف
تدمد:1872-8006
DOI:10.1016/j.bbagen.2019.02.001