Myeloid Cells in Traffic

such as circadian changes [4] but also under inflammatory conditions where disturbance of these axes induces increases in circulating myeloid cells and worsening of inflammatory diseases [5, 6] . The molecular mechanisms underlying the control of neutrophil homeostasis in steady-state and inflammatory conditions are reviewed in detail by Strydom and Rankin [7] . Neutrophils are the first leukocyte subset recruited to sites of inflammation. In the absence of microbial stimuli, i.e. in sterile inflammation, damage-associated molecular patterns (DAMPs) represent the trigger for neutrophil emigration. Important DAMPs are extracellular ATP [8, 9] , mitochondrial formylated peptides [10] and DNA [11] , all of which are released by dying cells. Here, Pittman and Kubes [12] summarize mechanisms by which DAMPs set off the neutrophil recruitment cascade in sterile inflammation. Once activated and adherent to the endothelium, neutrophils need to breach the endothelial barrier to reach the inflammatory site. Intercellular junctions connecting individual endothelial cells form a tight barrier, thus making paracellular transmigration a highly regulated process. This process is complemented by emerging alternative routes of transmigration such as transcellular migration and reverse transmigration [13] . Here, Daniel and van Buul [14] summarize the molecular mechanisms that regulate endothelial cell-cell junctions and prevent or permit leukocyte transendothelial migraAppearance of neutrophils and monocytes at the site of inflammation is a hallmark event during the inflammatory response. Trafficking of different leukocyte subsets requires a coordinated interaction of a variety of molecules in a process known as the leukocyte recruitment cascade. Classical descriptions of this multistep process consisted of leukocyte rolling, activation, adhesion and subsequent transmigration, involving selectins, cell adhesion molecules and chemokines as well as their respective receptors [1] . However, in recent years, this recruitment cascade has been refined by implementation of intermediate steps (e.g., adhesion strengthening and intraluminal crawling), discovery of tissue(e.g., in liver, lungs and large arteries) and leukocyte-specific (e.g., for classical vs. nonclassical monocytes) recruitment mechanisms, as well as by recognition of intercellular interactions (e.g., between leukocyte subsets). This special issue accommodates all these new developments in several review articles. Neutrophil homeostasis is maintained by a fine balance between granulopoiesis, retention in and release from the bone marrow as well as by clearance and destruction. Chemokine axes involving CXCR4 and CXCR2 are critically involved in the retention, mobilization and homing of neutrophils at sites of granulopoiesis [2, 3] . The importance of these axes in regulating myeloid cell homeostasis was shown under physiological conditions Published online: April 13, 2013 Journal of Innate Immunity