“One aspect revealed by our study is the role of the mouse G900 region in Th2 differentiation and allergic airway inflammation,” said Professor Hiroshi Nakajima, lead researcher on the study, in a press release. “This region, which is homologous to the human G900 region associated with asthma, has been shown to be essential for Th2 cell differentiation and allergic responses in vivo, particularly in the context of house dust mite (HDM)-induced allergic airway inflammation. Additionally, we demonstrated that this G900 region is important for optimizing three-dimensional chromatin structure near GATA3 in Th2 cells.”
Essentially, because the G900 region is no longer present, GATA3 cannot trigger the action of Th2, resulting in a lack of inflammatory response from the immune system, resulting in less inflammation in the body.
Results paving the way for potential new treatments
While the findings have uncovered new pathways that can be considered when developing targeted treatments for inflammatory asthma, much work still needs to be done to use the data in practical ways to help people living with the condition.
The next step is to find ways to regulate Th2 differentiation through restriction of the GATA3 enhancer in the genome. These adjustments may help reduce allergic asthma by interfering with the immune system's ability to take action against the allergens that cause asthma.
“By identifying and understanding important genetic regions that regulate immune responses, such as the mG900 region, it may be possible to develop precision medicine approaches tailored to an individual’s genetic profile. This could lead to more effective and personalized treatments, reduce the incidence and severity of allergic reactions and improve the quality of life of individuals suffering from these conditions,” Professor Nakajima added in a press release.