Deficiency of Small GTPase Rac2 Affects T Cell Activation

doi:10.1084/jem.194.7.915

Published online 24 September 2001. doi:10.1084/jem.194.7.915

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© The Rockefeller University Press, 0022-1007/2001/10/915/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 7, October 1, 2001 915-926

Original Article

Deficiency of Small GTPase Rac2 Affects T Cell Activation

Hong Yu^a,b, Dave Leitenberg^a,b, Baiyong Li^a, and Richard A. Flavell^a,b
^a Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
^b Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520

Correspondence to: Richard A. Flavell, Section of Immunobiology, Yale University School of Medicine, 310 Cedar St., FMB 412, New Haven, CT 06520. Tel:203-737-2216 Fax:203-737-2958 E-mail:richard.flavell{at}yale.edu.

Rac2 is a hematopoietic-specific GTPase acting as a molecularswitch to mediate both transcriptional activation and cell morphologicalchanges. We have examined the effect of Rac2 deficiency duringT cell activation. In Rac2^-/- T cells, proliferation was reducedupon stimulation with either plate-bound anti-CD3 or T cellreceptor–specific antigen. This defect is accompaniedwith decreased activation of mitogen activated protein kinaseextracellular signal–regulated kinase (ERK)1/2 and p38,and reduced Ca²+ mobilization. TCR stimulation–inducedactin polymerization is also reduced. In addition, anti-CD3cross-linking–induced T cell capping is reduced comparedwith wild-type T cells. These results indicate that Rac2 isimportant in mediating both transcriptional and cytoskeletalchanges during T cell activation. The phenotypic similarityof Rac2^-/- to Vav^-/- cells implicates Rac2 as a downstream mediatorof Vav signaling.

Key Words: T cell activation, Rac2, VAV, MAPK, cytoskeleton

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