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Biochim Biophys Acta Gen Subj. 2019 Feb 10. pii: S0304-4165(19)30027-3. doi: 10.1016/j.bbagen.2019.02.001. [Epub ahead of print]

Mercury-induced inflammation and autoimmunity.

Author information

1
Department of Molecular Medicine, Scripps Research, 10550 North Torrey Pines Road, La Jolla, CA, 92037, United States of America. Electronic address: mpollard@scripps.edu.
2
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.
3
Shiley Eye Institute, Department of Ophthalmology, University of California, San Diego, 9500 Gilman Drive #0946, La Jolla, CA 92093. Electronic address: cbtoomey@ucsd.edu.
4
Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden. Electronic address: per.hultman@liu.se.
5
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.

Abstract

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.

KEYWORDS:

Animal model; Autoimmunity; Human; Inflammation; Mercury

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