Causes: Sarcoidosis:
Unknown. Possibly autoimmune.
No one yet knows what causes sarcoidosis. The disease can appear suddenly and
disappear. Or it can develop gradually and go on to produce symptoms that come
and go, sometimes for a lifetime.
(Source: excerpt from NHLBI, Sarcoidosis: NHLBI)
Article excerpts about the
causes of Sarcoidosis:
Sarcoidosis is not a cancer. It is not contagious, and your friends and family will not catch it from you. Although it can occur in families, there is no evidence that sarcoidosis is passed from parents to children. (Source: excerpt from NHLBI, Sarcoidosis: NHLBI)
Originally, scientists thought that sarcoidosis was caused by an acquired state of immunological inertness (anergy). This notion was revised a few years ago, when the technique of bronchoalveolar lavage provided access to a vast array of cells and cell-derived mediators operating in the lungs of sarcoidosis patients. Sarcoidosis is now believed to be associated with a complex mix of immunological disturbances involving simultaneous activation, as well as depression, of certain immunological functions.
Immunological studies on sarcoidosis patients show that many of the immune functions associated with thymus-derived white blood cells, called T-lymphocytes or T-cells, are depressed. The depression of this cellular component of systemic immune response is expressed in the inability of the patients to evoke a delayed hypersensitivity skin reaction ( a positive skin test), when tested by the appropriate foreign substance, or antigen, underneath the skin.
In addition, the blood of sarcoidosis patients contains a reduced number of T-cells. These T-cells do not seem capable of responding normally when treated with substances known to stimulate the growth of laboratory-cultured T-cells. Neither do they produce their normal complement of immunological mediators, cytokines, through which the cells modify the behavior of other cells.
In contrast to the depression of the cellular immune response, humoral immune response of sarcoidosis patients is elevated. The humoral immune response is reflected by the production of circulating antibodies against a variety of exogenous antigens, including common viruses. This humoral component of systemic immune response is mediated by another class of lymphocytes known as B-lymphocytes, or B-cells, because they originate in the bone marrow.
In another indication of heightened humoral response, sarcoidosis patients seem prone to develop autoantibodies (antibodies against endogenous antigens) similar to rheumatoid factors.
With access to the cells and cell products in the lung tissue compartments through the bronchoalveolar technique, it also has become possible for researchers to complement the above investigations at the blood level with analysis of local inflammatory and immune events in the lungs.
In contrast to what is seen at the systemic level, the cellular immune response in the lungs seems to be heightened rather than depressed. The heightened cellular immune response in the diseased tissue is characterized by significant increases in activated T-lymphocytes with certain characteristic cell-surface antigens, as well as in activated alveolar macrophages.
This pronounced, localized cellular response is also accompanied by the appearance in the lung of an array of mediators that are thought to contribute to the disease process; these include interleukin-1, interleukin-2, B-cell growth factor, B-cell differentiation factor, fibroblast growth factor and fibronectin.
Because a number of lung diseases follow respiratory tract infections, ascertaining whether a virus can be implicated in the events leading to sarcoidosis remains an important area of research. Some recent observations seem to provide suggestive leads on this question. In these studies, the genes of cytomegalovirus (CMV), a common disease-causing virus, were introduced into lymphocytes, and the expression of the viral genes was studied. It was found that the viral genes were expressed both during acute infection of the cells and when the virus was not replicating in the cells. However, this expression seemed to take place only when the T-cells were activated by some injurious event.
In addition, the product of a CMV gene was found capable of activating the gene in alveolar macrophage responsible for the production of interleukin-1. Since interleukin-1 levels are found to increase in alveolar macrophage from patients with sarcoidosis, this suggests that certain viral genes can enhance the production of inflammatory components associated with sarcoidosis. Whether these findings implicate viral infections in the disease process in sarcoidosis is unclear. Future research with viral models may provide clues to the molecular mechanisms that trigger alterations in lymphocyte and macrophage regulation leading to sarcoidosis.
In 1995, the National Heart, Lung, and Blood Institute started a multicenter case control study of the etiology of sarcoidosis. The investigation is planned to last six years and will collect information and specimens for use in investigation of environmental, occupational, lifestyle, and genetic risk factors for sarcoidosis. Examination of the natural history of sarcoidosis is planned in patients at early and late stages of the disease. Such information should improve our understanding of the cause(s) of sarcoidosis and provide insight into how to better prevent and treat the disease. (Source: excerpt from NHLBI, Sarcoidosis: NHLBI)
As with all medical conditions, there may be many causal factors. Further relevant information on causes of Sarcoidosis may be found in:
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Sarcoidosis.
The cause of sarcoidosis is unknown, but these factors may play a role:
❑ hypersensitivity response (possibly from T-cell imbalance) to such agents as atypical mycobacteria, fungi, and pine pollen
❑ genetic predisposition (suggested by a slightly higher incidence of sarcoidosis within the same family)
❑ extreme immune response to infection.
Sarcoidosis occurs most commonly in adults ages 30 to 50. In the United States, sarcoidosis occurs predominantly among blacks, affecting twice as many women as men.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Although the cause of sarcoidosis is unknown, the following possible causes have been considered:
❑ hypersensitivity response (possibly from a T-cell imbalance) to such agents as atypical mycobacteria, fungi, and pine pollen
❑ genetic predisposition (suggested by a slightly higher incidence of sarcoidosis within the same family)
❑ chemicals, such as zirconium or beryllium, can lead to illnesses resembling sarcoidosis, suggesting an extrinsic cause for this disease.
Source: Handbook of Diseases, 2003
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