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Special Issue "Environmental Toxicants and Autoimmune Disease"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (15 June 2014)

Special Issue Editor

Guest Editor
Prof. Dr. Kathleen Gilbert

Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
Website | E-Mail
Interests: autoimmune disease; immunotoxicity; environmental pollutants; autoantibodies; oxidative stress; metabolism; toxicogenomics

Special Issue Information

Dear Colleagues,

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
Guest Editor

Submission

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs).


Keywords

  • autoimmune disease
  • immunotoxicity
  • environmental pollutants
  • autoantibodies
  • oxidative stress
  • metabolism
  • toxicogenomics

Published Papers (5 papers)

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Review

Open AccessReview Smoking and Rheumatoid Arthritis
Int. J. Mol. Sci. 2014, 15(12), 22279-22295; doi:10.3390/ijms151222279
Received: 27 August 2014 / Revised: 11 October 2014 / Accepted: 17 October 2014 / Published: 3 December 2014
Cited by 11 | PDF Full-text (694 KB) | HTML Full-text | XML Full-text
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease caused by both genetic and environmental factors. Smoking has been implicated as one of the most important extrinsic risk factors for its development and severity. Recent developments have shed light on the pathophysiology of RA
[...] Read more.
Rheumatoid arthritis (RA) is a chronic inflammatory disease caused by both genetic and environmental factors. Smoking has been implicated as one of the most important extrinsic risk factors for its development and severity. Recent developments have shed light on the pathophysiology of RA in smokers, including oxidative stress, inflammation, autoantibody formation and epigenetic changes. The association of smoking and the development of RA have been demonstrated through epidemiologic studies, as well as through in vivo and animal models of RA. With increased use of biological agents in addition to standard disease-modifying antirheumatic drugs (DMARDs), there has been interest in how smoking affects drug response in RA treatment. Recent evidence suggests the response and drug survival in people treated with anti-tumour necrosis factor (anti-TNF) therapy is poorer in heavy smokers, and possible immunological mechanisms for this effect are presented in the current paper. Full article
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)
Open AccessReview Targeting Dendritic Cell Function during Systemic Autoimmunity to Restore Tolerance
Int. J. Mol. Sci. 2014, 15(9), 16381-16417; doi:10.3390/ijms150916381
Received: 26 June 2014 / Revised: 29 August 2014 / Accepted: 5 September 2014 / Published: 16 September 2014
Cited by 10 | PDF Full-text (1152 KB) | HTML Full-text | XML Full-text
Abstract
Systemic autoimmune diseases can damage nearly every tissue or cell type of the body. Although a great deal of progress has been made in understanding the pathogenesis of autoimmune diseases, current therapies have not been improved, remain unspecific and are associated with significant
[...] Read more.
Systemic autoimmune diseases can damage nearly every tissue or cell type of the body. Although a great deal of progress has been made in understanding the pathogenesis of autoimmune diseases, current therapies have not been improved, remain unspecific and are associated with significant side effects. Because dendritic cells (DCs) play a major role in promoting immune tolerance against self-antigens (self-Ags), current efforts are focusing at generating new therapies based on the transfer of tolerogenic DCs (tolDCs) during autoimmunity. However, the feasibility of this approach during systemic autoimmunity has yet to be evaluated. TolDCs may ameliorate autoimmunity mainly by restoring T cell tolerance and, thus, indirectly modulating autoantibody development. In vitro induction of tolDCs loaded with immunodominant self-Ags and subsequent cell transfer to patients would be a specific new therapy that will avoid systemic immunosuppression. Herein, we review recent approaches evaluating the potential of tolDCs for the treatment of systemic autoimmune disorders. Full article
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)
Open AccessReview Environmental Factors, Toxicants and Systemic Lupus Erythematosus
Int. J. Mol. Sci. 2014, 15(9), 16043-16056; doi:10.3390/ijms150916043
Received: 23 June 2014 / Revised: 1 August 2014 / Accepted: 27 August 2014 / Published: 11 September 2014
Cited by 10 | PDF Full-text (759 KB) | HTML Full-text | XML Full-text
Abstract
Systemic lupus erythematosus (SLE) is an immune-complex-mediated multi-systemic autoimmune condition of multifactorial etiology, which mainly affects young women. It is currently believed that the onset of SLE and lupus flares are triggered by various environmental factors in genetically susceptible individuals. Various environmental agents
[...] Read more.
Systemic lupus erythematosus (SLE) is an immune-complex-mediated multi-systemic autoimmune condition of multifactorial etiology, which mainly affects young women. It is currently believed that the onset of SLE and lupus flares are triggered by various environmental factors in genetically susceptible individuals. Various environmental agents and toxicants, such as cigarette smoke, alcohol, occupationally- and non-occupationally-related chemicals, ultraviolet light, infections, sex hormones and certain medications and vaccines, have been implicated to induce SLE onset or flares in a number case series, case-control and population-based cohort studies and very few randomized controlled trials. Here, we will describe some of these recognized environmental lupus triggering and perpetuating factors and explain how these factors potentially bias the immune system towards autoimmunity through their interactions with genetic and epigenetic alterations. Further in-depth exploration of how potentially important environmental factors mechanistically interact with the immune system and the genome, which trigger the onset of SLE and lupus flares, will certainly be one of the plausible steps to prevent the onset and to decelerate the progress of the disease. Full article
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)
Open AccessReview Expert Panel Workshop Consensus Statement on the Role of the Environment in the Development of Autoimmune Disease
Int. J. Mol. Sci. 2014, 15(8), 14269-14297; doi:10.3390/ijms150814269
Received: 9 June 2014 / Revised: 31 July 2014 / Accepted: 4 August 2014 / Published: 15 August 2014
Cited by 17 | PDF Full-text (731 KB) | HTML Full-text | XML Full-text
Abstract
Autoimmune diseases include 80 or more complex disorders characterized by self-reactive, pathologic immune responses in which genetic susceptibility is largely insufficient to determine disease onset. In September 2010, the National Institute of Environmental Health Sciences (NIEHS) organized an expert panel workshop to evaluate
[...] Read more.
Autoimmune diseases include 80 or more complex disorders characterized by self-reactive, pathologic immune responses in which genetic susceptibility is largely insufficient to determine disease onset. In September 2010, the National Institute of Environmental Health Sciences (NIEHS) organized an expert panel workshop to evaluate the role of environmental factors in autoimmune diseases, and the state of the science regarding relevant mechanisms, animal models, and human studies. The objective of the workshop was to analyze the existing data to identify conclusions that could be drawn regarding environmental exposures and autoimmunity and to identify critical knowledge gaps and areas of uncertainty for future study. This consensus document summarizes key findings from published workshop monographs on areas in which “confident” and “likely” assessments were made, with recommendations for further research. Transcribed notes and slides were reviewed to synthesize an overview on exposure assessment and questions addressed by interdisciplinary panels. Critical advances in the field of autoimmune disease research have been made in the past decade. Collaborative translational and interdisciplinary research is needed to elucidate the role of environmental factors in autoimmune diseases. A focus on exposure assessment methodology is needed to improve the effectiveness of human studies, and more experimental studies are needed to focus on causal mechanisms underlying observed associations of environmental factors with autoimmune disease in humans. Full article
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)
Open AccessReview Iodine Excess as an Environmental Risk Factor for Autoimmune Thyroid Disease
Int. J. Mol. Sci. 2014, 15(7), 12895-12912; doi:10.3390/ijms150712895
Received: 19 June 2014 / Revised: 3 July 2014 / Accepted: 15 July 2014 / Published: 21 July 2014
Cited by 12 | PDF Full-text (695 KB) | HTML Full-text | XML Full-text
Abstract
The global effort to prevent iodine deficiency disorders through iodine supplementation, such as universal salt iodization, has achieved impressive progress during the last few decades. However, iodine excess, due to extensive environmental iodine exposure in addition to poor monitoring, is currently a more
[...] Read more.
The global effort to prevent iodine deficiency disorders through iodine supplementation, such as universal salt iodization, has achieved impressive progress during the last few decades. However, iodine excess, due to extensive environmental iodine exposure in addition to poor monitoring, is currently a more frequent occurrence than iodine deficiency. Iodine excess is a precipitating environmental factor in the development of autoimmune thyroid disease. Excessive amounts of iodide have been linked to the development of autoimmune thyroiditis in humans and animals, while intrathyroidal depletion of iodine prevents disease in animal strains susceptible to severe thyroiditis. Although the mechanisms by which iodide induces thyroiditis are still unclear, several mechanisms have been proposed: (1) excess iodine induces the production of cytokines and chemokines that can recruit immunocompetent cells to the thyroid; (2) processing excess iodine in thyroid epithelial cells may result in elevated levels of oxidative stress, leading to harmful lipid oxidation and thyroid tissue injuries; and (3) iodine incorporation in the protein chain of thyroglobulin may augment the antigenicity of this molecule. This review will summarize the current knowledge regarding excess iodide as an environmental toxicant and relate it to the development of autoimmune thyroid disease. Full article
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)

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