Nerve-immune cell interactions in the lungs cause allergic asthma

Allergic asthma, characterized by breathing difficulties triggered by inhaled allergens such as pollen, mould and pet dander, is the most common disease among children and can persist into adulthood. New research led by investigators at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), revealed the relationship between nerves and immune cells in the lungs.
The study, published in the Journal of Allergy & Clinical Immunology, generated unique newborn mouse models of allergen exposure that reproduce the progression of allergic asthma from childhood to adulthood. The work involved tracking allergen-specific immune cells called T helper 2 resident memory cells (Th2-TRMs) that are known to be the central mediator of recurrent allergic inflammation in the lungs.
“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.
He added, “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.”