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Environmental factors in autoimmune disease.


Autoimmune diseases Autoimmune diseases
A group of diseases, like rheumatoid arthritis and systemic lupus erythematosus, in which immune cells turn on the body, attacking various tissues and organs.

Mentioned in: Complement Deficiencies, Premature Menopause
 are chronic, potentially life-threatening conditions. There are more than 80 recognized autoimmune diseases including systemic lupus erythematosus Systemic Lupus Erythematosus Definition

Systemic lupus erythematosus (also called lupus or SLE) is a disease where a person's immune system attacks and injures the body's own organs and tissues. Almost every system of the body can be affected by SLE.
, glomerulonephritis glomerulonephritis: see nephritis. , multiple sclerosis, autoimmune thyroiditis autoimmune thyroiditis Hashimoto's disease, see there , rheumatoid arthritis rheumatoid arthritis

Chronic, progressive autoimmune disease causing connective-tissue inflammation, mostly in synovial joints. It can occur at any age, is more common in women, and has an unpredictable course.
, and myositis myositis

Inflammation of muscle tissue, often from bacterial, viral, or parasitic infection but sometimes of unknown origin. Most types destroy muscle and surrounding tissue. Bacteria may directly infect muscle (usually after injury) or produce substances toxic to it.
. Although some of the conditions afflict only small numbers of individuals, as a group autoimmune diseases represent an important public health concern. The common characteristics of these diseases are immune responses directed against healthy tissue or cellular components normally protected from immune attack and the resultant inflammatory response.

Although genetic susceptibility and exposure to infectious agents have been identified as possible contributors to autoimmune disease autoimmune disease, any of a number of abnormal conditions caused when the body produces antibodies to its own substances. In rheumatoid arthritis, a group of antibody molecules called collectively RF, or rheumatoid factor, is complexed to the individual's own gamma  and have been extensively studied, these factors cannot account for most cases. This suggests the likelihood of exposure to environmental agents as an etiologic factor, and research has linked environmental agents with autoimmunity. Human studies have shown an association with exposure to vinyl chloride, silica, and organic compounds. Likewise, experimental studies have shown numerous autoimmunity-related immunologic changes induced by exposure to metals, polycyclic aromatic hydrocarbons, and mycotoxins. Possible mechanisms for environmentally induced autoimmunity include molecular mimicry, alteration of lymphocyte signaling, and interference in the development of tolerance to self-antigens.

Despite the accumulation of these research data, there are still gaps in knowledge, including how to link results from human and animal studies. In February 2003, the NIEHS NIEHS National Institute of Environmental Health Sciences (NIH, DHHS) , along with other NIH "Not invented here." See digispeak.

NIH - The United States National Institutes of Health.
 institutes and centers, cosponsored a workshop titled "Environmental Factors in Autoimmune Disease." The goals of the workshop were to obtain input from the environmental health science and autoimmune research communities on the most appropriate and productive directions for research in the area of environmentally related autoimmune disease.

The workshop was attended by more than 100 participants, including basic scientists, epidemiologists, clinicians, and disease advocates, and included a session consisting of six breakout groups focused on the following topics: gene-environment interactions, altered antigens, immune modulations, signal transduction, translational research: systemic autoimmune disease, and translational research: organ-specific diseases. The meeting yielded two primary findings. First, although experimental animal data are strong, many more human studies, both epidemiologic and clinical, are needed to link environmental exposure to autoimmune disease. Second, greater efforts are needed to establish collaborations between epidemiologists and clinicians on the one hand, and basic scientists on the other.

The NIEHS is interested in receiving investigator-initiated applications in the area of environmental factors on autoimmunity.

Contact | J. Patrick Mastin, Ph.D., e-mail: mastin@niehs.nih.gov
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Title Annotation:NIEHS Extramural Update
Publication:Environmental Health Perspectives
Date:Jul 1, 2003
Words:389
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