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dc.contributor.authorCroker, B.en
dc.contributor.authorHandman, E.en
dc.contributor.authorHayball, J.en
dc.contributor.authorBaldwin, T.en
dc.contributor.authorVoigt, V.en
dc.contributor.authorCluse, L.en
dc.contributor.authorYang, F.en
dc.contributor.authorWilliams, D.en
dc.contributor.authorRoberts, A.en
dc.identifier.citationImmunology and Cell Biology, 2002; 80(3):231-240en
dc.description.abstractThe 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.en
dc.description.statementofresponsibilityBen A Croker, Emanuela Handman, John D Hayball, Tracey M Baldwin, Valentina Voigt, Leonie A Cluse, Feng-Chun Yang, David A Williams and Andrew W Robertsen
dc.publisherBlackwell Publishing Asiaen
dc.rights© 2002 Australasian Society for Immunologyen
dc.subjectchemotaxis; Rac2; T lymphocytes; TH1/TH2en
dc.titleRac2-deficient mice display perturbed T-cell distribution and chemotaxis, but only minor abnormalities in TH1 responsesen
dc.typeJournal articleen
pubs.library.collectionMedicine publicationsen
dc.identifier.orcidHayball, J. [0000-0002-3089-4506]en
Appears in Collections:Medicine publications

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