Jay K. Kolls

This study shows that IRF7 deficiency worsens influenza A disease in mice, independent of TLR7, by impairing early interferon responses and adaptive immunity.

This study uses a mouse model to show that rapid podocyte ablation leads to acute renal tubule cell necrosis, interstitial fibrosis, and renal failure.

This study shows that long-term ART in SIV-infected macaques reduces acute inflammation but maintains chronic macrophage and TLR-driven inflammation linked to vascular damage and aging.

This study uses scRNA-seq and flow cytometry to show that commensal microbes amplify sex-specific immune differences in the murine lung, with males showing myeloid bias and females lymphocyte skewing under SPF conditions.

The paper examines sex and race differences in human pancreatic islets using scRNA-seq and snATAC-seq, finding sex-specific gene expression and chromatin accessibility differences in β cells that change with type 2 diabetes.

This study examines the aerosol persistence of K. pneumoniae strains, finding that both laboratory and clinical strains remain viable for up to 32 hours in air.

This study examines how SIV-induced immunodeficiency affects SARS-CoV-2 infection in macaques, finding that while immune responses are impaired, viral kinetics and evolution remain unchanged.

This study shows that intermittent CMV infection in mice alters BBB metabolism and causes cognitive deficits, suggesting a potential role for pathogens in dementia progression.

The paper performs transcriptome analysis of human DIP lung tissue and identifies a GM-CSF signature, suggesting its involvement in DIP pathogenesis and highlighting immune cell contributions beyond alveolar macrophages.

BAMM-SC clusters droplet-based scRNA-seq data from multiple individuals by accounting for batch effects and heterogeneity, improving accuracy over existing methods.

The paper examines the chromatin landscape of nephron progenitors across age, identifying age-related changes in chromatin accessibility and regulatory regions that suggest old progenitors are epigenetically primed for differentiation.