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Dev Cell. 2016 Jul 25;38(2):135-46. doi: 10.1016/j.devcel.2016.06.023.

Diffusion Barriers, Mechanical Forces, and the Biophysics of Phagocytosis.

Author information

1
Program in Cell Biology, Peter Gilgan Centre for Research & Learning, Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada; Department of Biochemistry, University of Toronto, Toronto, ON M5S 1A8, Canada.
2
Program in Cell Biology, Peter Gilgan Centre for Research & Learning, Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada; Department of Biochemistry, University of Toronto, Toronto, ON M5S 1A8, Canada; Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, 290 Victoria Street, Toronto, ON M5C 1N8, Canada. Electronic address: sergio.grinstein@sickkids.ca.
3
Program in Cell Biology, Peter Gilgan Centre for Research & Learning, Hospital for Sick Children, 686 Bay Street, Toronto, ON M5G 0A4, Canada.

Abstract

Phagocytes recognize and eliminate pathogens, alert other tissues of impending threats, and provide a link between innate and adaptive immunity. They also maintain tissue homeostasis, consuming dead cells without causing alarm. The receptor engagement, signal transduction, and cytoskeletal rearrangements underlying phagocytosis are paradigmatic of other immune responses and bear similarities to macropinocytosis and cell migration. We discuss how the glycocalyx restricts access to phagocytic receptors, the processes that enable receptor engagement and clustering, and the remodeling of the actin cytoskeleton that controls the mobility of membrane proteins and lipids and provides the mechanical force propelling the phagocyte membrane toward and around the phagocytic prey.

KEYWORDS:

Arp2/3; CD44; CD45; Muc-1; dendritic cells; formin; macrophages

PMID:
27459066
DOI:
10.1016/j.devcel.2016.06.023
[Indexed for MEDLINE]
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