CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow.

By Kyle J. Eash, Adam M. Greenbaum, P. Gopalan, D. Link. Journal of Clinical Investigation, 2010

721 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/283ce20704dce4ec314d02d33d3126777b07f057

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Citations in the corpus

Neutrophils, from marrow to microbes. (2010, background): “The expression of SDF-1 by bone marrow endothelial cells is downregulated by G-CSF, whereas G-CSF upregulates their expression of KC and Grob, thus tilting the CCXR4-CXCR2 signaling in favor of CXCR2 and neutrophil release (Christopher et al., 2009; Eash et al., 2010) (Figure 1).”
Chemokines and chemokine receptors: positioning cells for host defense and immunity. (2014, background): “G-CSF also promotes increased expression of CXCL2 in bone marrow endothelium, actively promoting neutrophil exit (13).”
Rhythmic modulation of the hematopoietic niche through neutrophil clearance (2013, positive): “BM-derived neutrophils senesced ex vivo upregulate the expression of CXCR4, the receptor for CXCL12 which mediates their retention within and homing back to the BM (Eash et al., 2010; Eash et al., 2009; Martin et al., 2003; Suratt et al., 2001).”
Inflammation and aging: signaling pathways and intervention therapies (2023, background): “Another phenotypic change observed in neutrophils during in vitro culture is the downregulation of CXCR2 (CXCL1 receptor), a potent neutrophil chelator that has been shown to promote the release of neutrophils into the circulation and migration to sites of inflammation.(46,47) In mice, senescence ca”
Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types? (2018, background): “In addition, ligands for CXCR2, such as CXCL1, CXCL2, CXCL5, and CXCL8 (in humans) are expressed by endothelial cells outside the bone marrow when neutrophils need to be mobilized into the blood (Eash et al., 2010; Köhler et al., 2011).”
CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma (2016, positive): “The primary immune function of CXCR2 is the regulation of neutrophil migration, as it controls the egress of these cells from the bone marrow, and their recruitment to sites of inflammation (Cacalano et al., 1994; Eash et al., 2010).”
Tumor-associated neutrophils: friend or foe? (2012, neutral): “[40].”
The roles of vascular endothelial growth factor in bone repair and regeneration (2016, background): “Shortly after injury, the number of neutrophils in the peripheral circulation increases as neutrophil retention in the bone marrow is reduced by inflammatory stimuli [62].”
Monocyte recruitment during infection and inflammation (2011, background): “Granulocytes are retained in the bone marrow by CXCL12-mediated CXCR4 signalling and exit in response to CXCR2 ligands, such as CXCL2 (also known as MIP2) and CXCL1 (also known as KC), which are produced during infectio”
Role of the CXCL8-CXCR1/2 Axis in Cancer and Inflammatory Diseases (2017, positive): “CXCR2 is also involved in neutrophil trafficking from the bone marrow during development [124].”