Z. Lu

This study identifies interstitial macrophages as key drivers of chronic lung allograft dysfunction and suggests CSF1R as a therapeutic target.

This study identifies distinct pneumonia endotypes based on pathogen-specific host responses in the lung, linking them to clinical outcomes and suggesting personalized treatment strategies.

This study identifies and characterizes splenic macrophage subsets in mouse and human, revealing their ontogeny, dynamics, and age-related changes.

This study shows that influenza A infection accelerates the formation of disease-associated microglia in aging mice, with effects observed in white matter regions.

The paper identifies profibrotic monocyte-derived alveolar macrophages as a biomarker and therapeutic target in SSc-ILD by analyzing BAL fluid and lung explants.

This study identifies tissue-resident skeletal muscle macrophages that support muscle recovery from viral pneumonia in aging mice, with Mertk playing a key role.

The paper examines alveolar T cell responses in SARS-CoV-2 pneumonia patients, finding that early interferon signaling and targeting of structural proteins correlate with better clinical outcomes.

The paper shows that prolonged exposure to lung-derived cytokines in COVID-19 patients activates microglia, and corticosteroids reduce this inflammatory response.

The paper identifies profibrotic monocyte-derived alveolar macrophages and neutrophil recruitment as drivers of lung fibrosis in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19.

The paper identifies a positive feedback loop between SARS-CoV-2-infected alveolar macrophages and T cells in severe COVID-19 patients, driving persistent alveolitis.

ISRIB reduces pulmonary fibrosis severity in young and old mice by modulating stress response signaling in alveolar epithelial cells.

This study examines proteome changes in alveolar macrophages and type 2 cells from young and old mice before and after influenza infection, revealing age-related proteostasis and mitochondrial dysfunction that worsen with infection.

This study shows that the aging lung microenvironment shapes alveolar macrophage identity, influencing their phenotype during aging and after injury.