The scientific understanding of why some people are more susceptible to allergies than others is being strengthened by new studies. The University of Pennsylvania’s Perelman School of Medicine researchers discovered how genetic variations that change a particular protein called ETS1 can affect how our bodies react to allergens.
They discovered that in an animal model, even minor alterations in ETS1 can enhance the likelihood of allergic reactions that result in inflammation.
The results were reported in Immunity.
Allergies are the sixth most common cause of chronic illness in the United States, according to the Centers for Disease Control and Prevention, costing the country more than USD 18 billion annually. It is still unknown how our DNA can alter our chances of acquiring an allergy, despite the fact that prior research has proven a strong genetic basis for allergies and discovered specific genetic sequence differences that predispose for these chronic diseases. But realizing this might result in better research and perhaps even brand-new medicines.
By using modern genomics and imaging techniques, a collaborative team of researchers co-led by Penn’s Golnaz Vahedi, PhD, an associate professor of Genetics, and Jorge Henao-Mejia, MD, PhD, an associate professor of Pathology and Laboratory Medicine, found that the ETS1 protein plays a role in controlling a type of immune cell called CD4 T helper cells, which are important in allergic reactions and help orchestrate the immune response by activating and coordinating other immune cells.
DNA interactions within the genomic segment encompassing the ETS1 gene control how much of the ETS1 protein is made.
“We discovered that these interactions, work like a dimmer switch,” said Vahedi. “When there are changes in the DNA in this area, it can mess up the dimmer switch, causing problems with controlling the ETS1 protein. This can lead to imbalances in our immune cells and cause allergic inflammations.”
While there has been progress in understanding genetic traits that follow predictable patterns, like those passed down from parents, it’s been more challenging to understand conditions that involve many different genes and are common in populations. These complex conditions cannot be explained by simply “turning off” one gene. Instead, they may be caused by small changes in the DNA that affect how genes work together. However, researchers still do not know much about how these changes in DNA relate to how our genes are organized or how they affect how genes are expressed in most complex diseases.
“This work demonstrates how small differences in our DNA can disturb the balance between our immune cells, resulting in significant observable characteristics in patients. This phenomenon may occur in other common diseases such as autoimmune disorders,” said Henao-Mejia.
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