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Mercury-induced inflammation and autoimmunity
Scripps Res, CA 92037 USA.
Univ Calif San Diego, CA 92093 USA.
Univ Calif San Diego, CA 92093 USA.
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
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2019 (English)In: Biochimica et Biophysica Acta - General Subjects, ISSN 0304-4165, E-ISSN 1872-8006, Vol. 1863, no 12, article id UNSP 129299Article, review/survey (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
ELSEVIER , 2019. Vol. 1863, no 12, article id UNSP 129299
Keywords [en]
Mercury; Inflammation; Autoimmunity; Human; Animal model
National Category
Pharmacology and Toxicology
Identifiers
URN: urn:nbn:se:liu:diva-162307DOI: 10.1016/j.bbagen.2019.02.001ISI: 000495476600003PubMedID: 30742953OAI: oai:DiVA.org:liu-162307DiVA, id: diva2:1374081
Note

Funding Agencies|National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [ES021464, ES022625, ES027679, E5029263]

Available from: 2019-11-28 Created: 2019-11-28 Last updated: 2019-11-28

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