Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 194, Issue 7, Pages 915-925Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.194.7.915
Keywords
T cell activation; Rac2; VAV; MAPK; cytoskeleton
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Rac2 is a hematopoietic-specific GTPase acting as a molecular switch to mediate both transcriptional activation and cell morphological changes. We have examined the effect of Rac2 deficiency during T cell activation. In Rac2(-/-) T cells, proliferation was reduced upon stimulation with either plate-bound anti-CD3 or T cell receptor-specific antigen. This defect is accompanied with decreased activation of mitogen activated protein kinase extracellular signal-regulated kinase (EP-K) 1/2 and p38, and reduced Ca2+ mobilization. TCR stimulation-induced actin polymerization is also reduced. In addition, anti-CD3 cross-linking-induced T cell capping is reduced compared with wild-ty-pe T cells. These results indicate that Rac2 is important in mediating both transcriptional and cytoskeletal changes during T cell activation. The phenotypic similarity of Rac2(-/-) to Vav(-/-) cells implicates Rac2 as a downstream mediator of Vav signaling.
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