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 Blood, 15 October 2008, Vol. 112, No. 8, pp. 3048-3051.
Prepublished online as a Blood First Edition Paper on September 5, 2008; DOI 10.1182/blood-2008-02-135715.

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CHEMOKINES, CYTOKINES, AND INTERLEUKINS

Brief Report

PI3Kgamma (PI3K{gamma}) is essential for efficient induction of CXCR3 on activated T cells

Joseph Barbi1, Hannah E. Cummings1, Bao Lu2, Steve Oghumu1, Thomas Rückle3, Christian Rommel4, William Lafuse5, Caroline C. Whitacre5, and Abhay R. Satoskar1

1 Department of Microbiology, The Ohio State University, Columbus; 2 Ina Sue Perlmutter Laboratory, Children's Hospital, Harvard Medical School, Boston, MA; 3 Merck Serono International SA, Geneva, Switzerland; 4 Intellikine, La Jolla, CA; and 5 Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus

The gamma isoform of PI3Kinase (PI3K{gamma}) controls leukocyte chemotaxis by participating in GPCR signaling, and by regulating cellular polarization. Here we show that PI3K{gamma} is required for efficient induction of CXC chemokine receptor 3 (CXCR3) on T cells upon activation. T cells from PI3K{gamma}–/– mice up-regulated CXCR3 less efficiently than wild-type controls both upon activation in vitro as well as during Leishmania mexicana infection. Inhibition of PI3Kinases using wortmannin and LY294002 or blockade of PI3K{gamma} activity using a selective inhibitor or PI3K{gamma} siRNA suppressed induction of CXCR3 on T cells following activation. Levels of CXCR3 and T-bet mRNA were significantly lower in PI3K{gamma} inhibitor–treated T cells, indicating that PI3K{gamma} may control CXCR3 expression in part through induction of T-bet. These results reveal a novel role for PI3K{gamma} in the induction of CXCR3 on T cells and suggest that PI3K{gamma} may regulate leukocyte chemotaxis by controlling the expression of chemokine receptors.


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