The Journal of Experimental Medicine
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Published online 1 October 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 Yua,b, Dave Leitenberga,b, Baiyong Lia, and Richard A. Flavella,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
Section of Immunobiology, Yale University School of Medicine, 310 Cedar St., FMB 412, New Haven, CT 06520.203-737-2958203-737-2216

richard.flavell{at}yale.edu

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 (ERK)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-type 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.

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

D. Leitenberg's present address is George Washington University, Department of Immunology, Ross Hall Rm. 411, 2300 Eye St. NW, Washington, DC 20037.

B. Li's present address is Pfizer, Inc., East Point Rd., Groton, CT 06340.

Abbreviations used in this paper: ERK, extracellular signal–regulated kinase; JNK, c-Jun NH2-terminal kinase; KO, knockout; MAPK, mitogen-activated protein kinase; SMAC, supramolecular activation cluster; GEF, guanine nucleotide exchange factor.

© 2001 The Rockefeller University Press


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