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Cited by 556Neutrophil, Myeloperoxidase and Oxidative MechanismsProtein Kinase Regulation and GTPase SignalingChemokine receptors and signaling

Deficiency of the Hematopoietic Cell-Specific Rho Family GTPase Rac2 Is Characterized by Abnormalities in Neutrophil Function and Host Defense

Open access
Roberts, Andrew W., Kim, Chaekyun, Zhen, Ling, Lowe, John B., Kapur, Reuben, Petryniak, Bronislawa, Spaetti, Adam, Pollock, Jonathan D. +5 more·1999·Immunity
DOI 10.1016/s1074-7613(00)80019-9
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Abstract

In mammals, the Rho family GTPase Rac2 is restricted in expression to hematopoietic cells, where it is coexpressed with Rac1. Rac2-deficient mice were created to define the physiological requirement for two near-identical Rac proteins in hematopoietic cells. rac2-/- neutrophils displayed significant defects in chemotaxis, in shear-dependent L-selectin-mediated capture on the endothelial substrate Glycam-1, and in both F-actin generation and p38 and, unexpectedly, p42/p44 MAP kinase activation induced by chemoattractants. Superoxide production by rac2-/- bone marrow neutrophils was significantly reduced compared to wild type, but it was normal in activated peritoneal exudate neutrophils. These defects were reflected in vivo by baseline neutrophilia, reduced inflammatory peritoneal exudate formation, and increased mortality when challenged with Aspergillus fumigatus. Rac2 is an essential regulator of multiple specialized neutrophil functions.

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60 of 60 references verified0 citation errors · 0 not checkable

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  • Rac2 knockout mice display a number of hematopoietic defects mostly in blood cell-specific receptor function or hematopoietic-specific effector mechanisms and in kinase pathway-activated cell survival.

    “the Rac2 knockout mice display a number of hematopoietic defects mostly in the context of blood cell-specific receptor function or hematopoietic-specific effector mechanisms and also in kinase pathway-activated cell survival [1], [2], [6], [7], [8].”

    From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [6]

  • In the absence of Rac2, macrophages and/or neutrophils display defective chemotaxis.

    “Previous findings clearly demonstrate that in the absence of Rac2, macrophages and/or neutrophils display suppressed reactive oxygen species (ROS) production, defective chemotaxis, impaired phagocytosis, and decreased microbial killing [1], [2], [6], [7], [8].”

    From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [6]

  • In the absence of Rac2, macrophages and/or neutrophils display decreased microbial killing.

    “Previous findings clearly demonstrate that in the absence of Rac2, macrophages and/or neutrophils display suppressed reactive oxygen species (ROS) production, defective chemotaxis, impaired phagocytosis, and decreased microbial killing [1], [2], [6], [7], [8].”

    From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [6]

  • In the absence of Rac2, macrophages and/or neutrophils display impaired phagocytosis.

    “Previous findings clearly demonstrate that in the absence of Rac2, macrophages and/or neutrophils display suppressed reactive oxygen species (ROS) production, defective chemotaxis, impaired phagocytosis, and decreased microbial killing [1], [2], [6], [7], [8].”

    From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [6]

  • In the absence of Rac2, macrophages and/or neutrophils display suppressed reactive oxygen species (ROS) production.

    “Previous findings clearly demonstrate that in the absence of Rac2, macrophages and/or neutrophils display suppressed reactive oxygen species (ROS) production, defective chemotaxis, impaired phagocytosis, and decreased microbial killing [1], [2], [6], [7], [8].”

    From Rac2 Controls Tumor Growth, Metastasis and M1-M2 Macrophage Differentiation In Vivo (2014) · cites this paper as [6]

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Authors
Roberts, A. W., Kim, C., Zhen, L., Lowe, J. B., Kapur, R., Petryniak, B., Spaetti, A., Pollock, J. D., Borneo, J. B., Bradford, G. B., Atkinson, S. J., Dinauer, M. C., & Williams, D. A.
Affiliations
  • Howard Hughes Medical Institute (US)
  • Indiana University Indianapolis (US)
  • Indiana University School of Medicine (US)
Corresponding author
Williams, David A.
ORCID
Venue
Immunity
Publisher
Elsevier BV
Published
1999-02
Volume
10
Issue
2
Pages
183-196
ISSN
1074-7613 (ISSN-L)
DOI
10.1016/s1074-7613(00)80019-9
OpenAlex
W2010630254
Cited by
556
References
60
Citations by year
2026: 3 · 2025: 10 · 2024: 4 · 2023: 5 · 2022: 12 · 2021: 11 · 2020: 12 · 2019: 14 · 2018: 13 · 2017: 14 · 2016: 12 · 2015: 11 · 2014: 21 · 2013: 27 · 2012: 16
FWCI
10.60
Type
journal article
Language
en
Open access
Licence
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01hl052565-05)
  • U.S. Public Health Service (R01 45635)
  • National Heart, Lung, and Blood Institute (R01 HL52565)
  • National Cancer Institute (1P01 CA 71932, P01CA071932)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords
Rac2, Rho GTPases, hematopoietic cells, neutrophils, neutrophil chemotaxis, L-selectin, GlyCAM-1, F-actin, MAPK activation, superoxide production, neutrophilia, peritoneal exudate, Aspergillus fumigatus, host defense, Rac1
MeSH terms
Actins, Animals, Aspergillus, Chemotactic Factors, Cytoskeleton, Enzyme Activation, Hematopoiesis, Hematopoietic Stem Cells, Humans, Immunity, Neutrophils, Phosphorylation, Superoxides, Calcium-Calmodulin-Dependent Protein Kinases, GTP-Binding Proteins, Mitogen-Activated Protein Kinase 1, GTP Phosphohydrolases, rac GTP-Binding Proteins, Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Mice

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