Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2

By N. Serbina, Eric G. Pamer. Nature Immunology, 2006

1,760 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/6c1671a8163f7a2ce0cd68424a142df0bae40c2e

How researchers see this paper

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In Immunology

1. Steffen Jung
2. R. Ransohoff
3. A. Mildner
4. M. Guilliams
5. Florent Ginhoux
6. P. Murray
7. TA Wynn
8. P. Italiani

In Oncology

1. F. Geissmann
2. Eric G. Pamer
3. Peter Libby
4. A. Luster
5. R. Ransohoff
6. L. Chávez-Galán
7. I. Garcia
8. D. Vesin

Citations in the corpus

• Developmental and Functional Heterogeneity of Monocytes. (2018, background): “…monocytes are the TNF/iNOS-producing (Tip)-DC, which were originally identified in the spleen of mice during Listeria monocytogenes infection (Serbina et al., 2003), but could also detected in mice infected with the parasite Trypanosoma brucei (Bosschaerts et al., 2010; Guilliams et al.,…”
• Microglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions (2007, background): “A previous report claimed that the chemokine receptor CCR2 might also be required for the emigration of Ly-6C hi CCR2 + monocytes from the bone marrow into the circulatio”
• Critical roles for CCR2 and MCP-3 in monocyte mobilization from bone marrow and recruitment to inflammatory sites. (2007, neutral): “We have performed the adoptive transfer of monocytes approximately 60 hours after instillation of thioglycollate, as was done by Serbina and Pamer (32), and find that recruitment at this time point is CCR2 independent (data not shown).”
• Monocyte recruitment during infection and inflammation (2011, background): “Mice deficient in CCL2, CCL7 or CCR2 retain LY6C hi monocytes in the bone marrow, indicating that CCR2-mediated signals are principally required for LY6C hi monocyte recruitment from the bone marrow into the bloodstrea”
• Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis (2012, neutral): “As expected from the reported phenotype of Ccr2 −/− mice (Serbina and Pamer, 2006), in the blood Ly6C + Ccr2 −/− monocytes (CD45.”
• From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “During a bacterial infection, Ly6C monocytes require CCR2 for being recruited from the bone marrow into the blood (149).”
• Monocytes in atherosclerosis: subsets and functions (2010, background): “Chemokine receptors, in particular CCR2, are also important for the release of monocytes from the bone marrow”
• The fate and lifespan of human monocyte subsets in steady state and systemic inflammation (2017, background): “Classical monocytes are rapidly recruited to sites of infection (Serbina and Pamer, 2006; Liao et al., 2017) and injury (Nahrendorf et al., 2007; Zigmond et al., 2014), where they exhibit considerable functional plasticity (Arnold et al., 2007; Avraham-Davidi et al., 2013).”
• Alveolar macrophages develop from fetal monocytes that differentiate into long-lived cells in the first week of life via GM-CSF (2013, neutral): “As CCR2 is critical for egress of monocytes from the BM (Serbina and Pamer, 2006), competitive chimerism allowed us to address the relative contribution of circulating monocytes to AMF replenishment after whole body irradiation.”
• Therapeutic siRNA silencing in inflammatory monocytes (2011, background): “CCR2 also mediates egress of monocytes from the bone marro”
• Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells. (2012, background): “Monocyte-derived DCs emerge as important cellular players in the initiation or resolution of local adaptive immune reactions (Cheong et al., 2010; Lin et al., 2008; Serbina and Pamer, 2006).”