D. N. Kotton

This study identifies aberrant macrophage activation and maladaptive lung repair as key factors promoting tuberculosis progression in the lung using a novel mouse model.

This study generates human alveolar epithelial type I cells from iPSCs by activating YAP signaling, revealing Hippo-LATS-YAP's role in their differentiation.

This study compares the pathogenicity and immune evasion of an Omicron S-bearing virus with natural Omicron, showing vaccine escape via S mutations but severe disease due to factors outside S.

This study demonstrates the durable engraftment of PSC-derived lung epithelial cells into immunocompetent mice, showing long-term retention of both progenitor and differentiated cell phenotypes.

This study compares the transcriptomes of primary, cultured, and iPSC-derived human alveolar type 2 cells to assess how culture affects their gene expression profiles and maturation states.

The paper shows that nitazoxanide inhibits SARS-CoV-2 replication and pathogenesis in human and hamster models, and synergizes with remdesivir against multiple variants.

This study uses CRISPR-Cas9 to create syngeneic iPSC-derived hepatocytes with ZAAT heterozygosity, revealing metabolic dysregulation and cellular heterogeneity in MZ and ZZ cells.

This study identifies 17 FDA-approved compounds with antiviral efficacy against SARS-CoV-2 using high-throughput screening and finds lactoferrin as a promising drug candidate with multiple antiviral mechanisms.

This study uses recombinant Lloviu virus to investigate replication mechanisms and host interactions of an uncultured filovirus related to Ebola.

This study uses iPSC-derived airway cells to model SARS-CoV-2 infection, showing multiciliated cells as primary targets and demonstrating antiviral responses to remdesivir and camostat methylate.

This study uses patient-derived iPSCs with an SFTPC mutation to model early alveolar epithelial dysfunction in interstitial lung disease, revealing proteostasis, metabolic, and inflammatory changes.

This study identifies SARS-CoV-2 inhibition of the JAK-STAT pathway as a mechanism to suppress interferon signaling across diverse cell types.

This study investigates how SARS-CoV-2 interacts with host antiviral pathways in respiratory and cardiac cells, finding it activates OAS-RNase L and PKR but not IFN, contrasting with MERS-CoV.

This study uses iPSC-derived hepatic cells to show that liver proteostasis factors and UPR signaling correlate with TTR amyloid production and can reduce amyloid secretion through ER stress-independent activation.