Epigenetic underpinnings of developmental immunotoxicity and autoimmune disease

Abstract The concordance rate for developing autoimmune disease in identical twins is around 50% demonstrating that gene and environmental interactions contribute to disease etiology. The environmental contribution to autoimmune disease is a wide-ranging concept including exposure to immunotoxic environmental chemicals. Because the immune system is immature during development suggests that adult-onset autoimmunity may originate when the immune system is particularly sensitive. Among the pollutants most closely associated with inflammation and/or autoimmunity include Bisphenol-A, mercury, TCDD, and trichloroethylene. These toxicants have been shown to impart epigenetic changes (e.g., DNA methylation) that may alter immune function and promote autoreactivity. Here we review these autoimmune-promoting toxicants and their relation to immune cell epigenetics both in terms of adult and developmental exposure.