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The most prevalent chronic condition in children, allergic asthma can last into adulthood and is characterised by wheezing and breathing difficulties brought on by inhaled allergens such pollen, mould, and pet dander.
The interaction between nerves and immune cells in the lungs can play a role in the development of this disorder, according to new research undertaken by scientists at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB). For the study, which is published in the Journal of Allergy & Clinical Immunology. Unique newborn mouse models of allergen exposure that replicate the development of allergic asthma from childhood to adulthood were created by scientists. Tracking allergen-specific immune cells, also known as T helper 2 resident memory cells (Th2-TRMs), which are known to be the main cause of recurrent allergic inflammation in the lungs, was the focus of the research. Experiments revealed that sympathetic nerves in the lungs produce dopamine and reside in proximity to certain T helper 2 cells following allergen exposure in newborns. When dopamine binds to DRD4 receptors on these T helper 2 cells, the cells are more prone to be transformed into Th2-TRMs and are instructed to produce immune response-stimulating molecules, or cytokines. Blocking this dopamine binding following allergen exposure in newborns reduced the T helper 2 cell transformation and alleviated lung inflammation upon the encounter of the same allergen during adulthood. "Since human lungs are similarly innervated by dopaminergic nerves in early postnatal life, the dopamine-DRD4 axis may provide a therapeutic target to modify allergic asthma progression from childhood to adulthood," says senior author Xingbin Ai, PhD, an investigator at MGH and an associate professor of Pediatrics at Harvard Medical School. "Dopamine signaling is likely one of many age-related factors that regulate Th2-TRMs in the immature lung. Moving forward, it will be important to further delineate the molecular and functional features of the pathogenic Th2-TRMs generated in the immature lung. A better understanding of the mediators of the early life Th2-TRM program could identify new therapeutic targets for the treatment of allergic asthma." (ANI)
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