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Inflammatory bowel disease - Crohn's disease
Researchers do not know the exact causes of inflammatory bowel disease. IBD appears to be due to an interaction of many complex factors including genetics, impaired immune system response, and environmental triggers. The result is an abnormal immune system reaction, which in turn causes an inflammatory response in the body‚ ' s intestinal regions.
The Immune System's Infection Fighters. The primary infection-fighting units are two types of white blood cells: lymphocytes and leukocytes.
Lymphocytes include two subtypes known as T cells and B cells. Both types of cells are designed to recognize foreign invaders (antigens) and to launch an offensive or defensive action against them:
T cells are further categorized as killer T cells or helper T cells.
Helper T cells and Inflammatory Bowel Disease. The actions of the helper T cells (TH cells) are of special interest in inflammatory bowel disease:
Helper T cells are further categorized as TH1 and TH2. An imbalance in these two types appears to occur in IBD, although each disorder has a different balance.
Although the exact causes of inflammatory bowel disease are not yet known, genetic factors certainly play some role. Between 10 - 20% of people with ulcerative colitis have family members with the disease. Several identified genes and chromosome locations play a role in the development of ulcerative colitis, Crohn's disease, or both. Genetic factors appear to be more important in Crohn's disease, although there is evidence that both forms of inflammatory bowel disease have common genetic defects.
The first important genetic discovery for Crohn‚ ' s disease was the identification of the genetic variant CARD15 (also called NOD2), which alters the immune system so that it launches an over-reaction in response to bacteria, causing inflammation. However, this genetic factor only affects a small percentage of Crohn‚ ' s disease cases and is not involved with ulcerative colitis.
In recent years, scientists have made significant genetic research breakthroughs including identifying variants in interleukin-23 receptor (IL23R), which appears to be linked to increased or decreased risk for both Crohn‚ ' s disease and ulcerative colitis. Other genetic risk factors are also being investigated.
Measles. Some studies have reported that children with IBD may have had more and earlier childhood infections. The measles virus has been of particular interest. According to the U.S. Centers for Disease Control, and many studies, the measles virus does not cause Crohn‚ ' s or IBD.
Much publicity has centered on whether the vaccine for measles, mumps, and rubella (the MMR vaccine) causes conditions such as autism and Crohn‚ ' s disease. This theory has been rigorously reviewed and refuted in many well-conducted studies. The evidence clearly indicates that the MMR vaccine does not increase the risk of Crohn‚ ' s disease, other inflammatory bowel disease, or autism.
Inflammatory bowel disease is much more prevalent in industrialized nations and in higher-income groups. However, there is no strong evidence that diet or particular types of food cause Crohn‚ ' s disease or ulcerative colitis.
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