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Abstract Unlike that of T2 asthma, the pathophysiology of non–T2 asthma remains largely unexplored. However, increasing evidence supports a role for trained macrophages in asthma. In this study, we utilized a non-T2 asthma mouse model associated with early respiratory viral infection to identify the H3K27me3-NR1D1-IFN-γ axis in lung-trained macrophages, which drives non-T2 asthma by promoting Th1 differentiation.
Respiratory syncytial virus (RSV) is the main cause of acute lower respiratory tract infection (ALRI) in children worldwide. Virus-host interactions affect the progression and prognosis of the infection. Autophagy plays important roles in virus-host interactions. Respiratory epithelial cells serve as the front line of host defense during RSV infection, However, it is still unclear how they interact with RSV.
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