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

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 (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 TH1 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.

journal_name

Immunol Cell Biol

journal_title

Immunology and cell biology

authors

Croker BA,Handman E,Hayball JD,Baldwin TM,Voigt V,Cluse LA,Yang FC,Williams DA,Roberts AW

doi

10.1046/j.1440-1711.2002.01077.x

subject

Has Abstract

pub_date

2002-06-01 00:00:00

pages

231-40

issue

3

eissn

0818-9641

issn

1440-1711

pii

1077

journal_volume

80

pub_type

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