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International Immunology Advance Access originally published online on September 5, 2007
International Immunology 2007 19(11):1261-1270; doi:10.1093/intimm/dxm097
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Thymosin {alpha}1 activates the TLR9/MyD88/IRF7-dependent murine cytomegalovirus sensing for induction of anti-viral responses in vivo

Silvia Bozza1,2, Roberta Gaziano1, Pierluigi Bonifazi1, Teresa Zelante1, Lucia Pitzurra1, Claudia Montagnoli1, Silvia Moretti1, Roberto Castronari1, Paola Sinibaldi3, Guido Rasi4, Enrico Garaci5, Francesco Bistoni1,2 and Luigina Romani1,2

1 Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Via del Giochetto, 06122 Perugia, Perugia, Italy
2 Fondazione "Istituto di Ricovero e Cura per le Biotecnologie Trapiantologiche" I.B.i.T., Perugia, Italy
3 Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Tor Vergata, Rome, Italy
4 Institute of Neurobiology and Molecular Medicine, Centro Nazionale Ricerche, Rome, Italy
5 National Institute of Health, Rome, Italy

Correspondence to: L. Romani; E-mail: lromani{at}unipg.it

Reactivation of latent human cytomegalovirus following allogeneic transplantation is a major cause of morbidity and mortality and predisposes to severe complications. Thymosin {alpha}1 (T{alpha}1), a naturally occurring thymic peptide, is approved for treatment of some viral infections and as an immune adjuvant. T{alpha}1 successfully primed dendritic cells (DCs) for anti-microbial T helper type 1 resistance through Toll-like receptor (TLR) 9 signaling. We sought to determine here whether T{alpha}1 could play a role in murine cytomegalovirus infection (MCMV). To this purpose, susceptible, resistant and TLR-deficient mice were infected with MCMV, treated with T{alpha}1 and assessed for protection in term of microbiological and immunological parameters. T{alpha}1 protected susceptible and resistant mice from MCMV infection. The anti-viral effect of T{alpha}1 occurred through the activation of plasmacytoid DCs via the TLR9/myeloid differentiation primary response gene 88-dependent viral recognition sensing, leading to the activation of IFN regulatory factor 7 and the promotion of the IFN-{alpha}/IFN-{gamma}-dependent effector pathway.

Keywords: dendritic cells, immunomodulation, innate immunity, viral infections

Transmitting editor: S. Romagnani

Received 2 January 2007, accepted 7 August 2007.


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