B cells regulate production of neutrophils by a novel mechanism by releasing ST6Gal-1, an active sialyltransferase, that suppresses granulopoiesis.

Identification of distinct yolk sac-derived macrophage subpopulations in the fetal liver reveals their crucial role in shaping the hematopoietic niche, impacting erythropoiesis and granulopoiesis through direct interactions with long-term hematopoietic stem cells.

Linker histones affect the lineage determination of granulocyte precursor cells via regulation of the transcription factor GATA-2.

Perinatal granulopoiesis and cord blood serum PGLYRP-1, a specific granule protein, are altered prior to onset of childhood asthma and provide potential targets for early identification of at-risk populations.

In-silico modeling of gene and protein emergence reveals how colony-stimulating factors contributed to the evolution and functional adaptions observed in mammalian neutrophils.

LPS pre-exposure is tissue protective during a subsequent lethal E. coli peritonitis by long-term modulation the bone marrow B-cell and neutrophil pool which affects neutrophil tissue damaging properties and therapeutic activation of Cxcr4 promotes tissue damage control during sepsis.

Partial ablation of osteocytes alters lineage cell specifications in bone and bone marrow, resulting in the acceleration of skeletal aging.

Real-time visualization of Salmonella enterica and polarized macrophage interaction in the living host identifies an anti-inflammatory, pro-regenerative, and motionless macrophage subset as a survival niche during persistent infection.

Mycobacterium tuberculosis exploits an IFN/IL6/CEBP axis linked to monocyte expansion in humans.

The expansion of our understanding about the regulation of iron metabolism, erythropoiesis, and the crosstalk between them has enabled delineating the pathophysiology of multiple diseases and provided rationale for novel therapeutic interventions.