Fig. 3

Aged hosts display persistent inflammation and prolonged acute recovery following respiratory virus. The course of the respiratory infection in the aged host is characterized by prolonged recovery. Such impaired recovery program is in part attribute to the retention of neutrophils and the malfunction of AMs’ phagocytosis. The phenotypic skew of Tregs from reparative towards inflammatory is also important in the impaired recovery. Aged lungs also harbor significantly less ILC2s than the young lungs, accompanied by deficit in their pro-repair function. Aside from the immune compartment, ineffective regeneration of epithelial cells in aged hosts also contributes to their impaired reparative program. Krt5 + progenitor cells have been shown to accumulate in the aged lung following influenza virus infection