A new study has found that a mutation of the IL-33 gene may be the cause of food allergies, asthma and inflammation of the esophagus and skin. The researchers documented their observations and findings after studying a boy aged 12 who was found to have mutations of the interleukin 33 (IL-33) gene.
The study was conducted by a group of researchers led by Thomas Eiwegger. The Karl Landsteiner University health sciences professor stated that the most noticeable symptoms that confirmed IL-33’s role in immune system reactions included chronic inflammatory changes in the boy’s skin, eosinophilic esophagitis and chronic inflammation of the esophagus.
Up until recently, not much was known about IL-33’s in vivo function as studies had been limited to animal models and human-derived in vitro cellular models. The researchers’ discovery offers new insights into how IL-33 (interleukin 33) functions. IL-33 is a regulator of type-2 immune responses in the human body and is usually released after the body endures cellular damage.
While immune responses in the body usually help the body defend itself from bigger pathogens, they may sometimes cause allergic inflammation. The researchers recorded physical abnormalities of the boy, which included moderate developmental delay, short-sightedness, delayed growth in length with joint hypermobility, delayed weight gain, and changes in the face, jaw and cranial bones.
Eiwegger, who was recently appointed as the new head of St. Pölten University Hospital’s Department of Pediatrics and Adolescent Medicine, stated in the study’s report that all these abnormalities highlighted IL-33’s pleiotropic role. The researchers also found that the gene’s duplication affected IL-33’s concentration in some tissues as well as the blood, noting that increases in tissues of the skin and the gastrointestinal tract occurred even with no increase in IL-33’s actual concentration in the blood.
In addition to this, Eiwegger explained that the group observed varying subcellular localizations of the protein in a range of tissues, giving the example of its presence in the nuclei of inflamed tissue in the skin. This, the researchers said, suggested that IL-33 was tightly regulated in the body, arguing that this discovery could afford new explanations for tissue-specific illness patterns, which may in turn aid in the development of targeted therapies for illnesses that may have partly been caused by this protein.
Researchers hope that this discovery will aid in the development of better therapeutic options for patients afflicted by this mutation. The researchers also plan to investigate the use of monoclonal antibodies, which can bind to and eliminate IL-33 as options in studies for the treatment of food allergies, atopic dermatitis and asthma.
Many companies, such as Aditxt Inc. (NASDAQ: ADTX), are focused on finding effective treatments for conditions linked to immune system malfunction, and patients can only hope that these efforts yield positive outcomes sooner rather than later since many current treatments aren’t helping a great deal.
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