For about 1 in 100 people, foods that contain even the smallest amount of gluten can cause severe wounds and pose serious health risks.
Although the domino effect of immunological responses can be traced back to them Genetic rootsmany contributing factors are also involved, making it difficult to map the exact sequence of events that cause celiac disease.
Using transgenic mice, it has been led by an international team led by scientists at McMaster University in Canada Identified important roles The very cells that make up the intestinal lining play and explain the main stepping stones that could lead to new treatments.
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Celiac disease is a lifelong autoimmune disorder caused by the presence of a structural protein known in the intestine as gluten.
Eat virtually anything Made from wheat, barley or rye – meaning most baked goods, bread, and pasta – Someone with a condition There is a risk of temporary symptoms such as bloating, pain, diarrhea, constipation, and sometimes reflux and vomiting.
Currently, the only way to avoid symptoms is to avoid the foods that cause them. In the long term, immune attacks triggered by gluten cans Damages the villi of the small intestine. these Small structure It increases the internal surface area of the intestinal wall, which helps absorb nutrients from food.
People with celiac disease face serious health risks, such as being more likely to do so, especially if they are not treated Develops colorectal cancer and Cardiovascular disease. This disease is associated with countless conditions, anemia, osteoporosis, Growth delay, Reproductive problemsand Neuropathy.
“The only way to treat celiac disease today is to completely eliminate gluten from your diet.” say McMasters Gastroenterologist Elena Verdu.
“This is difficult and experts agree that gluten-free diets are insufficient.”
Approximately 90% of people diagnosed with this condition have a pair of protein-encoding genes HLA-DQ2.5. Of the remaining 10%, most have a similar protein called HLA-DQ8.
Like other types of “hla” (or Human leukocyte antigens) Proteins, proteins hold fragments of fallen invaders high like creepy trophies Immune cell classwarning other defensive organizations to keep an eye on it.
In certain cases of HLA-DQ2.5 and HLA-DQ8, the protein is shaped to retain a mass of digestively resistant gluten peptide, instructing murder T cells to go hunting.
Unfortunately, these instructions are least clear in distinguishing between similar materials from threats to our bodies. In other words, those with genes are at risk for a variety of autoimmune conditions.
Not everyone However, those who express either HLA-DQ2.5 or HLA-DQ8 develop immune disorders such as celiac disease.
To make it happen, those destroyed gluten fragments must first be carried across the intestinal wall. Transport of enzymes It binds to the peptide and changes it in a way that makes it more recognizable.
Cells in the intestinal wall are responsible for transporting this enzyme into the intestine, and thus play a clear important role in the early stages of the disease.
They are also known Represents a family of proteins HLA-DQ2.5 and HLA-DQ8 are usually regulated by inflammatory responses in the intestine.
What was not clear is how the basis for this staging actually works within the pathology itself for people with celiac disease.
To focus on this important link within the chain, the researchers reaffirmed the expression of cells that envelop people’s intestines with treated and untreated celiac disease, as well as major immune complexes in mice carrying the human gene of HLA-DQ2.5.
Mouse enterocytes were then used to create functional biological models of the intestine called organoids, and the expression of immune proteins was studied nearby, exposing them to inflammatory triggers and precedent intact gluten.
“This allowed us to narrow down specific causes and effects and prove exactly whether and how the reaction would occur.” say McMasters Biomedical Engineer Tohid Didar.
This revealed that cells lining the intestine are important agents that present mashups of broken gluten fragments in the intestine and transport enzymes to gluten specific immune cells, rather than passive bystanders who have made a false effort to remove the gluten body and suffered secondary collateral damage.
Knowing the types of tissues involved and their enhancement by the presence of inflammatory microorganisms will allow researchers to get a new list of targets for future treatments, allowing millions of people around the world to enjoy a gluten-filled pastry or two without the risk of discomfort.
This study was published in Gastroenterology.
An earlier version of this article was published in August 2024.
