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Rac2-deficient mice display perturbed T-cell distribution and chemotaxis, but only minor abnormalities in T(H)1 responses


Croker, BA; Handman, E; Hayball, JD; Baldwin, TM; Voigt, V; Cluse, LA; Yang, FC; Williams, DA; Roberts, AW
2002-06
IMMUNOLOGY AND CELL BIOLOGY
Journal Article
80
3
231-240
The haematopoietic-specific RhoGTPase, Rac2, has been indirectly implicated in T-lymphocyte development and function, and as a pivotal regulator of T Helper 1 (T(H)1) 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 T(H)1 responses in vivo , Rac2-deficient mice were challenged with Leishmania major and immunized with ovalbumin-expressing cytomegalovirus. Despite a minor skewing towards a T(H)2 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 T(H)1 responses to infection in vivo is largely redundant.
BLACKWELL PUBLISHING ASIA
MURINE CUTANEOUS LEISHMANIASIS; LYMPHOID ORGANS; B-CELLS; VAV PROTOONCOGENE; CYTOMEGALO-VIRUS; LIGAND CHEMOKINE; IMMUNE-RESPONSE; DEFICIENT MICE; ACTIVATION; GENE
10.1046/j.1440-1711.2002.01077.x
Refer to copyright notice on published article.

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Creation Date 2002-06-01 12:00:00