Rac2-deficient mice display perturbed T-cell distribution and chemotaxis, but only minor abnormalities in TH1 responses

Ben A. Croker, Emanuela Handman, John D. Hayball, Tracey M. Baldwin, Valentina Voigt, Leonie A. Cluse, Feng Chun Yang, David A. Williams, Andrew W. Roberts

Research output: Contribution to journalArticle

51 Scopus citations

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-γ 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.

Original languageEnglish (US)
Pages (from-to)231-240
Number of pages10
JournalImmunology and Cell Biology
Volume80
Issue number3
DOIs
StatePublished - Jun 26 2002

Keywords

  • Chemotaxis
  • Rac2
  • T lymphocytes
  • T1/T2

ASJC Scopus subject areas

  • Immunology
  • Clinical Biochemistry
  • Cell Biology

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