A histone acetyltransferase, known as E1A binding protein p300, appears to control asthma-related immune responses and airway inflammation.
Researchers found that p300 expression and histone acetyltransferase activity were significantly elevated in asthma cases, as outlined in the paper, “p300-Dependent Modulation in Regulatory T Cells Plays a Crucial Role in Allergic Asthma.” They used an allergen-induced asthma model in mice, which was validated with patient biopsy samples, and published their results in the American Journal of Respiratory and Critical Care Medicine.
According to the study, mice lacking p300 — either systemically or specifically in regulatory T cells (Tregs) — showed worsened allergic inflammation, reduced Treg populations and impaired Treg function. This led to heightened type-2 immune responses, which are central to asthma pathology.
Further analysis revealed that p300 directly influenced the expression of guanylate binding protein 5 (GBP5) in Tregs. GBP5 overexpression was able to restore Treg proliferation in p300-deficient conditions, suggesting a potential therapeutic target.
In reviewing the clinical implications of their study, researchers noted that p300 acts as a protective factor in allergic asthma by enhancing Treg function and suppressing Th2-driven airway inflammation. These findings open new avenues for epigenetic-based therapies aimed at improving immune regulation in asthma patients.
