Celiac disease: the causes of the disease and avoiding gluten

The causes of the disease are necessarily related to the consumption of gluten, but there is a genetic sensitivity. The genes found to be involved in the disease encode the creation of proteins called human tissue antigens (HLA)

The causes of the disease are necessarily related to the consumption of gluten, but there is a genetic sensitivity. The genes found to be involved in the disease encode the creation of proteins called human tissue antigens (HLA).

Almost all gout patients carry the DQ2 and DQ8 gene sets. However, about 30% of healthy people also carry these alleles. It is therefore clear that genetics is not the only reason for the outbreak of the disease, but there is a strong connection between the genes of the HLA system (immune system) and the incidence of leprosy. The immune overreaction begins when the protein fragments from the gluten are modified by the enzyme Tissue Transglutaminase (also known as tTG), which causes the acceleration of their binding to the proteins whose production is encoded by the DQ2 and DQ8 gene series. These present the protein fragments from the gliadin as foreign antigens to T immune cells, thus triggering the formation of an immune overreaction process and disease.

After diagnosing celiac disease, a gluten-free diet is required (avoiding eating bread, pasta, grains, etc.) for life; Even tiny amounts of gluten harm the restoration of the intestine. Many patients find it difficult to stick to such a limited diet. A special difficulty lies in the fact that many types of food, which are supposedly allowed for patients, may contain gluten residues and damage the recovering intestine. Thus, only half of the adults who adhere to a suitable diet for five years after a hernia diagnosis manage to fully restore the intestine.

Live with a pinch and consume gluten. possible?

The need to develop an alternative treatment that would save the requirement to avoid eating gluten motivated Robert Anderson and his colleagues from the Cancer Research Laboratory at the Walter and Eliza Hall Institute in Melbourne, Australia to investigate in detail how the T cells react to gluten and cause the immune overreaction in patients.

In July of this year, Anderson and his colleagues published their findings in the scientific journal Science Translational Medicine. The research in question began nine years ago, and with the help of various associations for gout patients, about 200 genetically predisposed patients from Australia and England were recruited. The researchers collected blood samples from the study participants six days after they ate food containing gluten. Using special methods developed in the laboratory, the T cells and the gliadin segments that caused the immune overreaction were isolated from the samples. Over 16,000 different protein segments originating from wheat, barley and rye were found, of which only 90 caused a T-cell response, and of which only three protein segments (peptides) were found to be particularly harmful.

The characterization of the protein segments from the gluten that stimulate the T cells will make it possible to conduct tests for food intended for celiac disease patients. In addition to this, the knowledge can be applied for the purpose of developing modern diagnostic methods and especially to develop treatment for these patients. Anderson is also the owner of the Australian company Nexpep, which is developing a drug for kidney disease. The company has developed a component that will expose the immune system to small amounts of the peptides identified in the study.

The researchers hope that with the help of small, controlled and repeated exposures, the immune system will eventually become tolerant to gluten. The intended drug is currently in the first phase of a clinical trial and results are expected in a few months.

Dina Volodarsky has a master's degree in life sciences from the Weizmann Institute of Science and a bachelor's degree in life sciences from the Hebrew University.

The full article was published in Galileo magazine, September 2010