Alexander V. Misharin

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 introduces expiMap, a deep learning model that enables interpretable reference mapping of single-cell transcriptome data by incorporating biologically meaningful gene programs.

The paper identifies a systemic age-dependent transcriptome imbalance driven by transcript length across multiple species and shows its correlation with splicing factors and environmental stressors.

This paper introduces scArches, a deep learning method for mapping query datasets onto reference single-cell atlases using transfer learning, effectively reducing batch effects and preserving biological information with fewer parameters.

The paper identifies a human accelerated region in Chromosome 14q12 that enhances forebrain expansion through increased enhancer activity in transgenic mice and organoids.

Single-cell RNA-seq of lung tissue from transplant donors, fibrosis patients, and a living patient identifies cell type-specific disease-associated molecular pathways in pulmonary fibrosis.

This study shows that β-catenin signaling negatively regulates Arginase 1 expression in lung macrophages, which may influence lung repair after injury.