Katharine M. Irvine

This study uses genetic biosensors to visualize calcium signaling dynamics in macrophages, revealing mechanosensitivity and the effects of Piezo1 channel ablation.

This study shows that mice with a germ-line deletion of a Csf1r enhancer lack specific macrophages but maintain normal physiology and can be replenished by donor cells.

This study shows that CSF1R-dependent macrophages are essential for hematopoiesis but many functions of tissue resident macrophages are redundant or strain-specific in mice.

This study shows that myeloid HDAC7 promotes liver inflammation and glucose dysregulation in obesity, using mouse models and human data.

This study shows that CHK1i+LDHU reprograms tumour-associated macrophages to an inflammatory state while preserving immunosuppressive features, enhancing CD8 T cell activation and therapeutic efficacy.

This study identifies a conserved regulatory element in the mouse Csf1r locus that contributes to transcription in hematopoietic and trophoblast cells, with partial redundancy with other enhancers.

This study uses spatial transcriptomics to analyze liver fibrosis stages in MASLD, identifying metabolic reprogramming and senescence signatures linked to fibrosis progression.

This paper tests whether perisurgical CSF1 treatment reduces liver I/R injury in rats by enhancing macrophage activity and liver regeneration.

This study examines the effects of a loss-of-function mutation in the rat Il34 gene on macrophage development, homeostasis, and inflammation in both the brain and periphery.

This study shows that wild-type bone marrow cells can restore macrophage populations and reverse developmental defects in Csf1rko rats, but not in the brain.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

This study examines the impact of a heterozygous Csf1r mutation on brain development and neuropathology in mice, showing reduced microglial abundance and altered gene expression in disease models.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.

This study shows that Csf1r mutation in mice, rats, and humans causes developmental defects, and bone marrow transfer can reverse some phenotypes by restoring macrophages.

This paper develops a CSF1R-FRed transgenic mouse that specifically labels mononuclear phagocyte system cells, showing high expression in monocytes, macrophages, and dendritic cells while excluding other lineages.

The paper reports a CRISPR-Cas9-induced deletion and reinsertion event in the mouse Csf1r promoter, highlighting the need for copy number analysis to confirm genomic edits.