Kathleen C.S. Cook

This study models early IAV infection in alveolar organoids, revealing conserved AT2 cell responses and uninfected cell state transitions driven by inflammation.

The paper shows that alveolar-basal intermediates (ABI) drive pulmonary fibrosis by coordinating a pro-fibrotic signaling niche in silicosis.

This study identifies biallelic LRRK2 loss-of-function variants as a cause of interstitial lung disease, showing reduced LRRK2 protein and impaired lung function in affected individuals.

The paper shows that the ARID1A-containing BAF complex is essential for lung development, proximal-distal axis specification, and cell fate acquisition during respiratory development.

This study shows that PRC2 maintains AT2 cell fate in the adult lung by preventing transitions to ABI and basal-like states, both in vitro and in vivo.