Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/9505
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Type: Journal article
Title: Rac2-deficient mice display perturbed T-cell distribution and chemotaxis, but only minor abnormalities in TH1 responses
Author: Croker, B.
Handman, E.
Hayball, J.
Baldwin, T.
Voigt, V.
Cluse, L.
Yang, F.
Williams, D.
Roberts, A.
Citation: Immunology and Cell Biology, 2002; 80(3):231-240
Publisher: Blackwell Publishing Asia
Issue Date: 2002
ISSN: 0818-9641
1440-1711
Statement of
Responsibility: 
Ben A Croker, Emanuela Handman, John D Hayball, Tracey M Baldwin, Valentina Voigt, Leonie A Cluse, Feng-Chun Yang, David A Williams and Andrew W Roberts
Abstract: The haematopoietic-specific RhoGTPase, Rac2, has been indirectly implicated in T-lymphocyte development and function, and as a pivotal regulator of T Helper 1 (TH1) responses. In other haematopoietic cells it regulates cytoskeletal rearrangement downstream of extracellular signals. Here we demonstrate that Rac2 deficiency results in an abnormal distribution of T lymphocytes in vivo and defects in T-lymphocyte migration and filamentous actin generation in response to chemoattractants in vitro. To investigate the requirement for Rac2 in IFN-gamma production and TH1 responses in vivo, Rac2-deficient mice were challenged with Leishmania major and immunized with ovalbumin-expressing cytomegalovirus. Despite a minor skewing towards a TH2 phenotype, Rac2-deficient mice displayed no increased susceptibility to L. major infection. Cytotoxic T-lymphocyte responses to cytomegalovirus and ovalbumin were also normal. Although Rac2 is required for normal T-lymphocyte migration, its role in the generation of TH1 responses to infection in vivo is largely redundant.
Keywords: chemotaxis
Rac2
T lymphocytes
TH1/TH2
Rights: © 2002 Australasian Society for Immunology
DOI: 10.1046/j.1440-1711.2002.01077.x
Appears in Collections:Aurora harvest 4
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