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The Journal of Immunology, 2004, 172: 6615-6625.
Copyright © 2004 by The American Association of Immunologists

Enhanced T Cell Proliferation in Mice Lacking the p85{beta} Subunit of Phosphoinositide 3-Kinase1

Jonathan A. Deane*, Matthew J. Trifilo*, Claudine M. Yballe{dagger}, Sangdun Choi{ddagger}, Thomas E. Lane* and David A. Fruman2,*

* Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697; {dagger} Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215; and {ddagger} Division of Biology, California Institute of Technology, Pasadena, CA 91125

Phosphoinositide 3-kinase activation is important for lymphocyte proliferation and survival. Disrupting the gene that encodes the major phosphoinositide 3-kinase regulatory isoform p85{alpha} impairs B cell development and proliferation. However, T cell functions are intact in the absence of p85{alpha}. In this study, we test the hypothesis that the related isoform p85{beta} is an essential regulatory subunit for T cell signaling. Unexpectedly, T cells lacking p85{beta} showed a marked increase in proliferation and decreased death when stimulated with anti-CD3 plus IL-2. Both CD4+ and CD8+ T cells completed more cell divisions. Transcriptional profiling revealed reduced levels of caspase-6 mRNA in p85{beta}-deficient T cells, which was paralleled by reduced caspase-6 enzyme activity. Increased T cell accumulation was also observed in vivo following infection of p85{beta}-deficient mice with mouse hepatitis virus. Together, these results suggest a unique role for p85{beta} in limiting T cell expansion.




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