The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
Tyrosine phosphorylation of the intracellular domain of LRP1 serves as a molecular switch to regulate cellular cholesterol homeostasis through nuclear hormone receptor-mediated regulation of the cellular cholesterol exporter ABCA1.
Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.
Francisella tularensis spreads from cell to cell when macrophages engulf small portions of infected cells upon cell contact, forming distinctive a double membraned endosome containing multiple bacteria per individual vacuole.
Large-volume light microscopy combined with higher-resolution electron tomography revealed the spatial distribution of virus-producing cells and highlighted mechanisms of HIV-1 dissemination in bone marrow from a small animal model.
Resident dermal Mφ are programmed locally, independently of bone-marrow monocytes during Staphylococcus aureus infection, leading to transiently increased resistance, which is limited by a decrease in macrophage life span.
In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.