What is Autoimmune Disease?
Autoimmune disease is a group of disorders characterized by abnormal immune responses to normal tissue or organs. These reactions are caused by an overactive immune system. The body’s own defenses against infection and other threats are overwhelmed by the increased activity of the immune system. This leads to inflammation, which may lead to scarring, loss of function, and even death.
The term “autoimmunity” was first used in the late 19th century to refer to these conditions.
In general, autoimmunity refers to any condition in which the immune system attacks healthy tissues without provocation. There are two main categories: Type I (proto) autoimmune diseases and Type IIa (antibody) autoimmune diseases. Type I autoimmune diseases include such conditions as lupus, rheumatoid arthritis, psoriasis, scleroderma, multiple sclerosis (MS), and juvenile idiopathic arthritis. Type IIa autoimmune diseases include such conditions as systemic lupus erythematosus (SLE), Sjögren’s syndrome, celiac sprue and non-Hodgkin lymphoma.
Autoantibodies are antibodies made by the immune system that are directed against a person’s own tissues, and are found in most cases of autoimmune disease.
A related concept is that of dysregulation, a condition in which the immune system shows over- or under-activity in the absence of an autoimmune disease. A number of conditions have features of dysregulation, such as asthma, celiac disease, and inflammatory bowel disease. It is also a feature of many types of cancer.
Autoimmune diseases such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis, and others are believed to have a strong genetic basis. Some types appear to run in families (such as type 1 diabetes and celiac disease), while other types (such as rheumatoid arthritis) typically do not. There are certain people who are more likely to develop autoimmune disorders than others; these people seem to have a genetic susceptibility to autoimmunity.
It is commonly believed that genetics plays a major role in the development of autoimmune diseases. Indeed, many of these diseases have a clear inheritance pattern. For example, individuals with a family history of type 1 diabetes mellitus (T1DM) are much more likely to develop the disease than those without such a family history. It is not clear, however, how this inheritance pattern manifests.
It has also been observed that autoimmune diseases tend to occur with greater frequency within some families than in the general population. This suggests a genetic link, since environment is unlikely to be the cause of such diseases within a family; rather, it is likely a combination of genetics and environment (see below). Finally, some autoimmune diseases can be prevented by removing the affected individual from their environment and into a more sterile environment.
Multiple factors interact in determining whether a person develops an autoimmune disease or not. It has been suggested that the critical factor is genetics, and environment just acts to either initiate symptoms in a predisposed individual or enhance the effects of the condition. This is supported by the fact that many autoimmune diseases are known to occur in isolated populations (such as Stó:lõ), in which genes are relatively homogeneous. Within these populations, there is a greater incidence of autoimmune and other genetic-based diseases (such as cystic fibrosis, Duchenne muscular dystrophy).
In addition to these “pure” genetic factors, outside factors are thought to play a role in autoimmune disease. These include viral infections, exposure to toxic chemicals (including cigarette smoke), and others.
Some scientists believe the hygiene hypothesis may be an explanation for the rise in certain autoimmune diseases such as hay fever and asthma. The hygiene hypothesis states that since our environment is increasingly clean and free of disease-causing organisms, our immune systems never learn how to fight off diseases, and begin attacking the body itself by mistake.
Evidence is growing for an association between infections and autoimmune diseases. Pathogens can cause an immune response that may lead to long-lasting changes in the immune system. One explanation is that a common set of genes makes some people vulnerable to both infectious disease and autoimmune disease.
There are several possible ways in which infection may cause autoimmunity. The first is that viruses cause direct damage to the immune system, the second is the generation of autoimmune antibodies against host antigens, and the third is a bystander activation of autoreactive T cells by infectious dendritic cells.
More recent evidence points to a virus as the cause of nearly all cases of insulin-dependent diabetes. It has been suggested that while most people can fight off this virus, those with a certain set of genes that cause a predisposition for autoimmune disease are unable to fight it off, and thus become diabetic.
Helminths are parasites that infect humans, such as tapeworms and other similar organisms. In areas of the world with low prevalence of parasites, there is a higher occurrence of autoimmune diseases. This suggests that helminths actively suppress inappropriate immune responses, in a manner similar to the way vaccines do. It is thought that the increase in autoimmune disease in industrialized nations is the result of decreasing exposure to these organisms.
It has been suggested that a virus may be linked to multiple sclerosis.
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