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Comment
. 2021 Dec 6;6(1):416.
doi: 10.1038/s41392-021-00836-5.

Neutrophil swarm control: what goes up must come down

Stefan Uderhardt #  1   2   3 , Jasmin Knopf #  4   5 , Martin Herrmann #  1   2
Affiliations
Comment

Neutrophil swarm control: what goes up must come down

Stefan Uderhardt et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Neutrophil fates under homeostatic or inflammatory conditions. Neutrophils arise from precursor cells in the bone marrow and are released into the bloodstream, from where they set out to patrol the internal tissues as well as the ocular surfaces and exocrine ducts. Under homeostatic conditions (green box), neutrophils undergo different fates: (a) NET formation and excretion, (b) in situ apoptosis or (c) re-circulation to the bone marrow and clearance. Under inflammatory conditions (red box), neutrophils are attracted to the site of infection or damage (d) first through a sequential combination of long- and short-ranging chemoattractants. The latter mediates the coordinated extravascular aggregation dynamics known as swarming behavior. Kienle et al. now show that preprogrammed desensitization of the very G-protein-coupled receptors (GPCRs) that drive swarming is an intrinsic feedback control that leads to dynamic arrest (e). This arrest ensures stable cluster formation and is critical for their antibacterial effector functions. Successful elimination of the invading pathogen is then followed by apoptosis in situ and elimination by recruited phagocytes (f), which is the trigger for the active resolution of inflammation
See this image and copyright information in PMC

Comment on

  • Neutrophils self-limit swarming to contain bacterial growth in vivo.
    Kienle K, Glaser KM, Eickhoff S, Mihlan M, Knöpper K, Reátegui E, Epple MW, Gunzer M, Baumeister R, Tarrant TK, Germain RN, Irimia D, Kastenmüller W, Lämmermann T. Kienle K, et al. Science. 2021 Jun 18;372(6548):eabe7729. doi: 10.1126/science.abe7729. Science. 2021. PMID: 34140358 Free PMC article.

References

    1. Kienle K, et al. Neutrophils self-limit swarming to contain bacterial growth in vivo. Science. 2021;372:eabe7729. doi: 10.1126/science.abe7729. - DOI - PMC - PubMed
    1. Freeman SA, et al. Lipid-gated monovalent ion fluxes regulate endocytic traffic and support immune surveillance. Science. 2020;367:301–305. doi: 10.1126/science.aaw9544. - DOI - PMC - PubMed
    1. Uderhardt S, Martins AJ, Tsang JS, Lämmermann T, Germain RN. Resident macrophages cloak tissue microlesions to prevent neutrophil-driven inflammatory damage. Cell. 2019;177:541–555.e17. doi: 10.1016/j.cell.2019.02.028. - DOI - PMC - PubMed
    1. Schauer C, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat. Med. 2014;20:511–517. doi: 10.1038/nm.3547. - DOI - PubMed
    1. Knopf J, Leppkes M, Schett G, Herrmann M, Muñoz LE. Aggregated NETs sequester and detoxify extracellular histones. Front. Immunol. 2019;10:2176. doi: 10.3389/fimmu.2019.02176. - DOI - PMC - PubMed

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