In a novel cell-in-cell interaction termed emperipolesis, neutrophils routinely transit through the cytoplasm of bone marrow megakaryocytes to pass surface membrane to newly-generated hybrid platelets.
Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.
Blood flow-driven shear forces guide the sequential signaling of two antagonistic paired receptors, a critical bi-facet step that first supports leukocyte docking, then initiates transmigration through endothelium.
The interaction between activated αIIbβ3 on platelets and SLC44A2 on circulating neutrophils facilitates neutrophil capture and drives flow-dependent NETosis.
The use of genetically encoded redox sensors in phagocytized bacteria reveals that, among the toxic cocktail of oxidants released into the neutrophil's phagolysosome, HOCl is the main component responsible for the oxidative modification of bacterial protein thiols.
Neutrophil pseudopods are composed of multiple sheets that are inherently flat, protrude in three dimensions, and whose assembly correlates with cell turning.
Targeting the differentiation regulators and/or AMPs of keratinocytes, rather than targeting immune cells, may be an alternative approach for topical anti-psoriatic treatment, an area with high need for new drugs.
The collective dynamics of cell signaling relays are at once dramatically sensitive to the system dimensionality and insensitive to many biological details.
