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Rac2‐deficient mice display perturbed T‐cell distribution and chemotaxis, but only minor abnormalities in T H 1 responses
Author(s) -
Croker Ben A,
Handman Emanuela,
Hayball John D,
Baldwin Tracey M,
Voigt Valentina,
Cluse Leonie A,
Yang FengChun,
Williams David A,
Roberts Andrew W
Publication year - 2002
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.2002.01077.x
Subject(s) - biology , cytotoxic t cell , t lymphocyte , immunology , microbiology and biotechnology , chemotaxis , haematopoiesis , in vivo , immune system , in vitro , stem cell , biochemistry , genetics , receptor
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‐γ 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.