Croker, B.Handman, E.Hayball, J.Baldwin, T.Voigt, V.Cluse, L.Yang, F.Williams, D.Roberts, A.2006-06-262006-06-262002Immunology and Cell Biology, 2002; 80(3):231-2400818-96411440-1711http://hdl.handle.net/2440/9505The 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© 2002 Australasian Society for ImmunologychemotaxisRac2T lymphocytesTH1/TH2Journal article002002075310.1046/j.1440-1711.2002.01077.x0001765724000042-s2.0-003598934360186Hayball, J. [0000-0002-3089-4506]