Yuefeng Huang, PhD

Asthma is a chronic disease resulting from complex interaction between genetics and environmental factors. It is a significant cause of illness in adults as well as the most frequent cause of hospitalization in young children. Immune cells called type 2 innate lymphoid cells (ILC2s) are a driver of asthma development. They secrete large amounts of inflammation-causing cytokine proteins that trigger too many white blood cells called eosinophils and mucus production. Our preliminary studies found that an RNA modification called m6A is critical to regulating this exaggerated ILC2 response. We will investigate how m6A controls ILC2 expansion and cytokine production during allergic asthma. We will identify any potential association between abnormal m6A activities and occurrence of certain asthma subtypes. These studies will significantly advance the understanding of asthma development and open up a new avenue for diagnosis and treatment to this disease.

Update: Our team has developed innovative animal models to explain the critical role of m6A RNA modification in asthma development. We demonstrated that m6A markedly worsens allergic asthma by intensifying immune responses of two types of immune cells, innate ILC2s and adaptive Th2 cells. Our findings uncover a previously unrecognized yet pivotal layer of immune regulation in asthma. This offers profound insights into its molecular underpinnings and identifies m6A as a potential therapeutic target for asthma.