By using modern genomics and imaging techniques, researchers 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 Golnaz Vahedi, Associate Professor of Genetics, at the varsity’s Perelman School of Medicine.
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“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 inflammation,” she added.
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.
Small Changes in DNA Could Equal Big Changes in Immune Cells
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 Jorge Henao-Mejia, Associate Professor of Pathology and Laboratory Medicine at the Perelman.
Reference :
- Quantitative control of Ets1 dosage by a multi-enhancer hub promotes Th1 cell differentiation and protects from allergic inflammation – (https://www.cell.com/immunity/fulltext/S1074-7613(23)00221-2)
Source: IANS
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