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 Blood, 9 April 2009, Vol. 113, No. 15, pp. 3520-3529.
Prepublished online as a Blood First Edition Paper on December 1, 2008; DOI 10.1182/blood-2008-07-171942.

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Submitted July 31, 2008
Accepted November 4, 2008

Viperin is required for optimal Th2 responses and T cell receptor-mediated activation of NF-{kappa}B and AP-1

Lian-Qun Qiu, Peter Cresswell, and Keh-Chuang Chin*

Laboratory of Gene Regulation and Inflammation, Singapore Immunology Network, Biomedical Sciences Institutes, Singapore, Singapore
Department of Immunobiology, Yale University School of Medicine, New Haven, CT, United States

* Corresponding author; email: kehchuang_chin{at}immunol.a-star.edu.sg.

Viperin has been identified as a highly inducible endoplasmic reticulum (ER) protein that has antiviral activity. Here we characterized the phenotype of mice deficient in viperin and examined the biological function of viperin in peripheral T cell activation and differentiation. Splenic CD4+ T cells deficient in viperin exhibited normal anti-TCR-induced proliferation and IL-2 production, but produced significantly less Th2 cytokines including IL-4, IL-5 and IL-13, in association with impaired GATA3 activation, after stimulation with anti-CD3 antibody, which was not restored upon costimulation with anti-CD28. Th2 differentiation of viperin-deficient naive T cells was also impaired in the presence of strong TCR signaling and minimum IL-4, but not under optimal Th2-skewed conditions. In parallel, viperin-deficient T cells showed decreases in NF-{kappa}B1/p50 and AP-1/JunB DNA binding activities after TCR engagement. Thus, viperin facilitates TCR-mediated GATA-3 activation and optimal Th2 cytokine production by modulating NF-{kappa}B and AP-1 activities.


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 Proc. Natl. Acad. Sci. USAHome page
E. R. Hinson and P. Cresswell
The antiviral protein, viperin, localizes to lipid droplets via its N-terminal amphipathic {alpha}-helix
PNAS, December 1, 2009; 106(48): 20452 - 20457.
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