Special Issue "Environmental Toxicants and Autoimmune Disease"
Deadline for manuscript submissions: 15 June 2014
Prof. Dr. Kathleen Gilbert
Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
Interests: autoimmune disease; immunotoxicity; environmental pollutants; autoantibodies; oxidative stress; metabolism; toxicogenomics
It is estimated that up to 8% of the population in the US, predominantly women, have one or more autoimmune disease. Some autoimmune diseases are life-threatening; all are debilitating and require lifelong medical care. Preventing these diseases requires a better understanding of their ill-defined and seemingly complex etiology. Although there is clearly a genetic component, the concordance rate for developing a particular autoimmune disease in identical twins is usually much less than 50%. This is interpreted to mean that environmental factors also contribute to disease etiology. The environmental contribution to autoimmune disease has come to include contact with certain chemicals that impact the immune system. Most chemicals tested for immunotoxicity appear to suppress the immune system. However, there are several types of environmental chemicals, including certain heavy metals, asbestos and chlorinated solvents that appear to inappropriately stimulate the immune system in a manner that promotes autoimmune diseases and other types of hypersensitivity reactions. This has been demonstrated in epidemiological studies as well as rodent models, and encompasses occupational as well as environmental exposure. Especially compelling are new studies suggesting that developmental exposure to certain toxicants may be even more likely than adult exposure to promote later-life autoimmunity. Toxicants can stimulate a specific immune response to chemically altered self-proteins, or can promote autoimmunity via antigen non-specific pro-inflammatory means. They can impact different cellular components of the immune system and can work at different levels ranging from epigenetic to protein structure. Articles in this Special Issue will present research aimed at characterizing the mechanisms by which environmental toxicants contribute to autoimmune disease.
Prof. Dr. Kathleen Gilbert
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.
- autoimmune disease
- environmental pollutants
- oxidative stress
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Iodide and autoimmune thyroiditis
Authors: Yuqian Luo, Akira Kawashima, Yuko Ishido, Kenzaburo Oda, Naoki Hiroi, Tetsuhide Ito, Norihisa Ishii and Koichi Suzuki
Abstract: The thyroid gland is one of the major organs targeted for autoimmune attack. Like cancers, it is assumed that autoimmune thyroid disease develops due to an interaction of a numbers of genetic factors and environmental factors. Iodine has been shown to be one precipitating environmental factor that contributes to the development of autoimmune thyroid diseases. It has been shown that, excessive amounts of iodide have been linked to the development of autoimmune thyroiditis in human and animals, while intrathyroidal depletion of iodine prevents disease in animal strains susceptible to severe thyroiditis. Although the mechanisms by which iodide promotes thyroiditis is still not fully understood, several hypotheses have been proposed. (1) High dose of iodide induces chemokine production that may recruit immunocompetent cells to the thyroid. (2) Iodine incorporation in the thyroglobulin may augment the antigenicity of this molecule. (3) A defect in the iodine processing machinery in thyroid epithelial cells may result in elevated levels of oxidative stress, leading to lipid and protein damage. This review will summarize the current knowledge regarding the involvement of iodide in autoimmune thyroid disease.
Keywords: iodide, autoimmune thyroiditis, environmental factors, and oxidative stress
Title: Environmental factors, toxicants and systemic lupus erythematosus
Authors: Anselm Mak
Affiliation: Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore
Abstract: Systemic lupus erythematosus (SLE) is an immune-complex mediated autoimmune condition of multifactorial aetiology which carries substantial morbidity and mortality. It is currently believed that the onset of SLE is probably triggered by various environmental factors in genetically susceptible individuals. While a number of lupus susceptible genes has been identified during the past 2 decades, various potential environmental agents which may induce SLE have been implicated in a number of case-control and population-based cohort studies. In this Review, we will discuss a number of environmental factors which may contribute to the onset and perpetuation of SLE, such as cigarette smoke, alcohol intake, occupationally and non-occupationally related chemicals, ultraviolet light, hormones, infections and vaccines. Although a cure of SLE will probably not materialize in the very near future, further in-depth exploration of how important environmental factors mechanistically interact with the immune system and the genome which potentially trigger the onset of SLE and its disease progression will certainly be one of the initial steps to prevent the onset and decelerate the progression of the disease.
Last update: 17 March 2014