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Journal of Immunology Research
Volume 2015, Article ID 235170, 15 pages
http://dx.doi.org/10.1155/2015/235170
Review Article

Regulators and Effectors of Arf GTPases in Neutrophils

1Division of Infectious Diseases and Immunology, CHU de Quebec Research Center, Quebec, QC, Canada G1V 4G2
2Faculty of Medicine, Laval University, Quebec, QC, Canada G1V 0A6

Received 11 August 2015; Accepted 30 September 2015

Academic Editor: Clifford Lowell

Copyright © 2015 Jouda Gamara et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Polymorphonuclear neutrophils (PMNs) are key innate immune cells that represent the first line of defence against infection. They are the first leukocytes to migrate from the blood to injured or infected sites. This process involves molecular mechanisms that coordinate cell polarization, delivery of receptors, and activation of integrins at the leading edge of migrating PMNs. These phagocytes actively engulf microorganisms or form neutrophil extracellular traps (NETs) to trap and kill pathogens with bactericidal compounds. Association of the NADPH oxidase complex at the phagosomal membrane for production of reactive oxygen species (ROS) and delivery of proteolytic enzymes into the phagosome initiate pathogen killing and removal. G protein-dependent signalling pathways tightly control PMN functions. In this review, we will focus on the small monomeric GTPases of the Arf family and their guanine exchange factors (GEFs) and GTPase activating proteins (GAPs) as components of signalling cascades regulating PMN responses. GEFs and GAPs are multidomain proteins that control cellular events in time and space through interaction with other proteins and lipids inside the cells. The number of Arf GAPs identified in PMNs is expanding, and dissecting their functions will provide important insights into the role of these proteins in PMN physiology.