Lyle L. Moldawer

The paper profiles chromatin accessibility in post-sepsis MDSCs, showing divergent epigenetic trajectories between rapid recovery and chronic critical illness, with MHC class II repression in CCI.

This study identifies prolonged reduced oxidative metabolism and mitochondrial mass in CD66b+ leukocytes from sepsis patients, linked to adverse outcomes and gene silencing.

This study identifies a biphasic epigenetic and transcriptional response in macrophages after burn injury, revealing locus-specific chromatin remodeling and immune dysfunction.

This study examines age and sex effects on MDSCs in sepsis using single-cell RNA sequencing, finding differences in expansion, transcriptome, and metabolism.

The paper identifies a novel framework to quantify immune dysregulation in critical illness by analyzing transcriptomic data across multiple cohorts.

This study maps epigenetic changes in MDSCs after sepsis, revealing age- and sex-specific chromatin remodeling linked to immune dysfunction.

This study uses ELISpot to assess immunomodulatory drug effects on cytokine production in sepsis patients and healthy controls.

This study shows RvD2/GPR18 signaling enhances M-MDSC function to reduce AAA formation by suppressing inflammation and vascular remodeling.

This study shows that MerTK-dependent efferocytosis by monocytic-MDSCs reduces post-lung transplant ischemia-reperfusion injury.

This study develops and optimizes a diluted whole blood ELISpot assay to assess immune function in septic patients, showing it can measure cytokine responses under various conditions.

This study uses ELISpot to track changes in innate and adaptive immunity during sepsis and shows it can detect immune therapy effects.

The paper develops gene-expression-based prognostic models for 30-day mortality in sepsis using community-onset and hospital-acquired sepsis cohorts, showing improved prediction when combined with clinical scores.