Florent Ginhoux

This study identifies the role of mature dendritic cells type 1 in forming, maintaining, and functioning tertiary lymphoid structures in cancer.

Renoir maps ligand-target activities across spatial topologies and identifies context-specific cell-cell interactions from spatial transcriptomics data.

The paper identifies distinct transcriptional and epigenetic profiles of brain-engrafted monocyte-derived macrophages compared to microglia, showing their origin from peripheral blood and skull bone marrow.

The paper demonstrates that delivering FLT3L with CXCL9 and CCL5 enhances cDC1 infiltration and antitumor immunity in mice and humanized models.

The paper identifies a novel macrophage-like population in exocrine glands sustained by ILC2-derived GM-CSF, showing conservation across species.

Novae is a graph-based foundation model for spatial transcriptomics that improves domain inference and batch correction across multiple tissues and technologies.

This study shows that systemic FAK inhibition reduces immunosuppressive macrophages in glioblastoma by blocking monocyte trafficking, enhancing T cell activity and improving survival in a mouse model.

The paper identifies NRF2-driven myeloid progenitor dysregulation that sustains immunosuppressive macrophages in tumors, showing NRF2 inhibition reduces their survival and enhances antitumor immunity.

This study shows that co-culturing iPSC-derived macrophages with hepatocytes enhances macrophage maturation and hepatocyte function through direct cell-cell contact.

The paper investigates how rabies virus interacts with different human brain cell types, identifying a pro-viral astrocyte subpopulation that enhances viral transcription.

The paper identifies CCR7+ dendritic cells as the primary source of IL-23 in psoriasis, linking them to type 17 inflammation and relapse.

The paper identifies a tricellular niche in the cornea involving macrophages, nerves, and Schwann cells that supports Piezo2-mediated touch sensation.

This study identifies Cpa3-expressing precursors as the source of embryonic mast cells, independent of granulocyte-monocyte progenitors, using single-cell RNA sequencing and genetic fate mapping.

This study uses brain organoids to model HDLS, showing that CSF-1R mutations in microglia lead to metabolic changes and inflammation that impair neuronal cells.

This study identifies a novel inflammation-associated dendritic cell state in human chronic inflammation and shows its spatial restriction and therapeutic relevance.

This study presents lineage tracing results from 18 myeloid-specific fate-mapping models in mouse peripheral blood and synovial tissue, validating synovial macrophage identification through flow cytometry and CITE-seq.

The paper identifies resident tissue macrophages as critical for maintaining intraocular pressure homeostasis by regulating extracellular matrix turnover in the trabecular meshwork.

This study identifies early yolk sac-derived macrophages in the pituitary gland and shows their role in hormonal regulation and post-pubertal gene expression.

This study shows that the Arp2/3 complex is essential for genome integrity and survival of epidermal Langerhans cells, with Arpc4 deficiency leading to DNA damage and premature aging-like decline.

Sopa provides a technology-invariant pipeline for analyzing image-based spatial-omics data, offering unified visualization and analysis tools.

This study examines how stroke alters myeloid cell composition and phenotypes in the brain, linking changes to cell origin, spatial organization, and brain connectivity.

This study shows that Ermin deficiency causes myelin abnormalities and inflammation, leading to neurological deficits and increased susceptibility to demyelination, suggesting it as an 'inside-out' model for inflammatory dysmyelination.

The paper uses scRNA-seq to identify TROP2+ liver progenitor cells co-expressing ACE2 and TMPRSS2, suggesting they may be targets for SARS-CoV-2 infection and contribute to COVID-19-associated liver dysfunction.

This study shows that expanded CAG repeats in HTT disrupt neural progenitor expansion and differentiation in human cerebral organoids, suggesting abnormal neurodevelopment in Huntington disease.

This study shows that CSF-1 signaling is essential for cerebellar microglia identity and function, and its disruption causes motor and social behavior defects.

This study shows that prenatal inflammation and macrophage depletion affect PV interneuron wiring in two distinct ways during development and adulthood, leading to altered inhibitory circuit function.

The paper investigates how microbiota affects myelination and white matter plasticity in a Huntington disease mouse model, finding altered myelin thickness and oligodendrocyte numbers in germ-free conditions.

The paper evaluates UMAP as an alternative to t-SNE for single-cell data, finding it faster, more consistent, and better at preserving cluster organization and continuums.

This study identifies nine distinct microglial states in mice across lifespan and after injury using single-cell RNA sequencing, revealing persistent and age-related changes.