Environmental triggers of autoimmune thyroiditis

Abstract

Autoimmune thyroiditis is among the most prevalent of all the autoimmunities. Autoimmune thyroiditis is multifactorial with contributions from genetic and environmental factors. Much information has been published about the genetic predisposition to autoimmune thyroiditis both in experimental animals and humans. There is, in contrast, very little data on environmental agents that can serve as the trigger or autoimmunity in a genetically predisposed host. The best-established environmental factor is excess dietary iodine. Increased iodine consumption is strongly implicated as a trigger for thyroiditis, but only in genetically susceptible individuals. However, excess iodine is not the only environmental agent implicated as a trigger leading to autoimmune thyroiditis. There are a wide variety of other synthetic chemicals that affect the thyroid gland or have the ability to promote immune dysfunction in the host. These chemicals are released into the environment by design, such as in pesticides, or as a by-product of industry. Candidate pollutants include polyaromatic hydrocarbons, polybrominated biphenols, and polychlorinated biphenols, among others. Infections are also reputed to trigger autoimmunity and may act alone or in concert with environmental chemicals. We have utilized a unique animal model, the NOD.H2 h4 mouse to explore the influence of iodine and other environmental factors on autoimmune thyroiditis.

Infectious Agents and Xenobiotics in the Etiology of Primary Biliary Cirrhosis

“…xenobiotics) that can either alter or complex to a defined self or non-self protein, causing a change in its molecular structure that induces an immune response. This fascinating hypothesis has been proposed for numerous autoimmune diseases, particularly based on the observed geoepidemiological gradient [50,120,121] in which definitive confirmation is awaited and should not be considered as exclusive with regard to the role of infectious agents. The hypothesis is supported by a number of epidemiology studies, as previously discussed, as well as by the appearance of autoantibodies in subjects immunized with halothane, an inhalatory anesthetic no longer used, with antibodies crossreacting with lipoylated PDC-E2 [122].…”

Thyroid Disruptors: How They Act and How We React

“…Most of these findings may be reversed after iodine withdrawal (Mizukami et al 1993). In vivo studies showed that while excess iodine is not necessary for the induction of thyroiditis, the ingestion of excess iodine works to exacerbate autoimmune thyroiditis in this genetically predisposed population (Burek and Talor 2009). Clearly, excess iodine intake has many roles in thyroid dysfunction, and one of these roles is to increase thyroglobulin immunogenicity (Papanastasiou et al 2007), while another is to increase adhesion molecules on the thyrocyte itself (Sharma et al 2005;Sharma et al 2008).…”

Study of Antithyroid Peroxidase Antibodies in People with Normal Range Thyroid Stimulating Hormone

“…7 The exposure to environmental toxicants such as polyaromatic hydrocarbons or polyhalogenated biphenyls, both are commonly used in a variety of industrial applications, have been shown to provoke thyroid autoimmunity not only in experimental animals but also in humans. 8 Several autoimmune disorders have been reported to be associated with autoimmune thyroiditis and may coexist with other organ-specific autoantibodies. 9 Tolerance to self antigen is obtained by elimination of autoreactive T-cells 10 and defect in this mechanism leads to activation of these cells and consequent autoimmunity.…”