Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage
Uderhardt S, Martins AJ, Tsang JS, Lammermann T, Germain RN (2019)
Publication Type: Journal article
Publication year: 2019
Journal
Book Volume: 177
Pages Range: 541-555.e17
Journal Issue: 3
DOI: 10.1016/j.cell.2019.02.028
Abstract
Neutrophils are attracted to and generate dense swarms at sites of cell damage in diverse tissues, often extending the local disruption of organ architecture produced by the initial insult. Whether the inflammatory damage resulting from such neutrophil accumulation is an inescapable consequence of parenchymal cell death has not been explored. Using a combination of dynamic intravital imaging and confocal multiplex microscopy, we report here that tissue-resident macrophages rapidly sense the death of individual cells and extend membrane processes that sequester the damage, a process that prevents initiation of the feedforward chemoattractant signaling cascade that results in neutrophil swarms. Through this “cloaking” mechanism, the resident macrophages prevent neutrophil-mediated inflammatory damage, maintaining tissue homeostasis in the face of local cell injury that occurs on a regular basis in many organs because of mechanical and other stresses. Video Abstract:[Figure presented]
Authors with CRIS profile
Involved external institutions
US National Institutes of Health (NIH)
United States (USA) (US)
Max-Planck-Institut für Immunbiologie und Epigenetik (MPI-IE) / Max Planck Institute of Immunobiology and Epigenetics
Germany (DE)
United States (USA) (US)
Max-Planck-Institut für Immunbiologie und Epigenetik (MPI-IE) / Max Planck Institute of Immunobiology and Epigenetics
Germany (DE)
How to cite
APA:
Uderhardt, S., Martins, A.J., Tsang, J.S., Lammermann, T., & Germain, R.N. (2019). Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage. Cell, 177(3), 541-555.e17. https://doi.org/10.1016/j.cell.2019.02.028
MLA:
Uderhardt, Stefan, et al. "Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage." Cell 177.3 (2019): 541-555.e17.
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