For about one in one hundred, foods even containing the smallest quantities of gluten can offer an injury and present serious risks to their health.
While a domino effect of immunological reactions can be traced genetic rootsA Number of contributory factors are also involved, which makes it difficult to map the precise event chain which causes celiac disease.
Use of transgenic mice, an international team led by scientists from McMaster University in Canada identified a crucial role Played by the cells very constituting the lining of the intestine, describing a major springboard that could lead to new therapies.
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Coeliac disease is an autoimmune lifetime disorder triggered by the presence of a group of structural proteins called gluten in the intestines.
Eat practically anything Made with wheat, barley or rye – which means most pastries, breads and pasta – people with the condition At risk of transient symptoms such as bloating, pain, diarrhea, constipation and sometimes reflux and vomiting.
Currently, the only way to avoid symptoms is to avoid foods that trigger them. In the longer term, immune attacks triggered by gluten can damage the villi of the small intestine. These tiny structures increase the internal surface of the intestinal walls, which AIDS Absorption of food nutrients.
People with celiac disease – especially if they are not treated – are faced with serious health risks, such as being more likely to Develop colorectal cancer And cardiovascular disease. The disease is associated with a myriad of conditions, with only a few examples, in particular anemia,, osteoporosis,, growth delays,, Reproduction problemsAnd neurological disorders.
“The only way to treat celiac disease today is to fully eliminate gluten from the” “diet” said Gastroenterologist McMasters Elena Verdu.
“This is difficult to do, and experts agree that a gluten -free diet is insufficient.”
About 90% of people diagnosed with the condition bear a pair of genes that code for a protein called HLA-DQ2.5. Of the remaining 10%, most have a similar protein called HLA-DQ8.
Like other types of “HLA” (or Human leukocyte antigen) Proteins, proteins contain invaders who have fallen at altitude like macabre trophies on a immune cell classwarning other defensive fabrics to be on the lookout.
In the specific case of HLA-DQ2.5 and HLA-DQ8, the proteins are shaped to contain pieces of gluten peptide that resist digestion, asking the TIGRIERS T cells to hunt.
Unfortunately, these instructions are not the clearest to distinguish a threat and materials of similar appearance in our body, which means that those with genes are at risk of a variety of autoimmune conditions.
Not everyone which expresses HLA-DQ2.5 or HLA-DQ8, however, will develop an immune disorder such as celiac disease.
For this to happen, these torn gluten pieces must first be transported through the intestinal wall by a transport enzyme which binds to the peptide and modifies it so as to make it even more recognizable.
The cells of the intestinal wall are responsible for the release of this transport enzyme in the intestine, so that they clearly have an essential role in the first stages of the disease.
They are also known for express the protein family To which HLA-DQ2.5 and HLA-DQ8 belong, which are generally regulated by inflammatory responses in the intestine.
What was not clear is how this staging ground for people with celiac disease actually works within the pathology itself.
To focus on this important link in the chain, the research team has doubled the expression of the main immune complex in cells that line the intestines of people with treated and untreated celiac disease, and in mice with human genes for HLA-DQ2.5.
They then created live functional models of the intestine, called organoidUsing intestinal mouse cells, to study the expression of their immune proteins closely, subjecting them to inflammatory triggers as well as predigated and intact gluten.
“This allowed us to reduce the specific cause and effect and prove exactly if and how the reaction takes place”, ” said Biomedical engineer McMasters Tohid Didar.
From this, it has become clear that the cells aligning the intestine were not only passives suffering from collateral damage in an erroneous effort to rid the body of gluten – they were key agents, with a mixture of gluten fragments decomposed by intestinal bacteria and the transport of enzymes with specific immune cells.
Knowing the types of tissues involved and their improvement by the presence of inflammatory microbes gives researchers a new list of targets for future treatments, potentially allowing millions of people worldwide to enjoy a pastry filled with gluten or two without risk of discomfort.
This research was published in Gastroenterology.
A previous version of this article was published in August 2024.