In a dramatic illustration of the potential for microbes to prevent disease, researchers at Yale University and the University of Chicago showed that mice exposed to common stomach bacteria were protected against the development of Type I diabetes.
The findings, reported in the journal Nature, support the so-called "hygiene hypothesis" – the theory that a lack of exposure to parasites, bacteria and viruses in the developed world may lead to increased risk of diseases like allergies, asthma, and other disorders of the immune system. The results also suggest that exposure to some forms of bacteria might actually help prevent onset of Type I diabetes, an autoimmune disease in which the patient's immune system launches an attack on cells in the pancreas that produce insulin.
In a completely different study, scientists have made a breakthrough on the genetic side:
New research from Stanford University scientists suggests that type 1 diabetes, an autoimmune disease that develops in children and young adults, may not be due to bad genes but rather to good genes behaving badly.
Because type 1 diabetes typically runs in families, scientists have looked for inborn genetic errors or gene variants passed on from generation to generation. Although this search has failed to find a single type 1 diabetes gene, many candidate type 1 diabetes susceptibility genes have been identified. These susceptibility genes, located in a region known as the major histocompatibility complex (MHC), help the body distinguish its own cells and tissues from those that are foreign.
[...] According to Dr. Fathman, the results suggest that type 1 diabetes may not result from genetic mutations but from differences in how normal genes and gene variants are turned on and off during disease progression. In addition to identifying altered genes that may indicate potential avenues for therapeutic or preventive treatments, the authors also found patterns of coordinated gene expression that may prove useful as biomarkers of disease onset or progression.
1 comment:
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