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The ssRNA Genome of Human Rhinovirus Induces a Type I IFN Response but Fails to Induce Maturation in Human Monocyte-Derived Dendritic Cells¹

Catharina Schrauf^*,¶, Stefanie Kirchberger^*,||, Otto Majdic^*, Maria Seyerl^*, Gerhard-Johann Zlabinger^*, Karl Manfred Stuhlmeier, Monika Sachet, Joachim Seipelt and Johannes Stöckl^2,*

^* Institute of Immunology, Department of Surgery, Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, and Ludwig Boltzmann Institute for Rheumatology and Balneology, Vienna, Austria; ^¶ Institute of Infection Immunology, Twincore, Centre for Experimental and Clinical Infection Research, Hanover, Germany; and ^|| Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom

Dendritic cells (DCs) use pattern recognition receptors to sense invading viruses and triggering of these receptors induces a maturation program. Human rhinoviruses (HRVs) belong to the family of Picornaviridae, which have a single-stranded, coding RNA genome. Because HRV does not replicate in DCs, we used genomic RNA from HRV in this study to analyze the impact of natural occurring viral ssRNA on DC function. We found that transfection of human monocyte-derived DCs with viral ssRNA induced type I IFN production but failed to activate the NF-B pathway in DCs. In line with this observation, the up-regulation of typical maturation markers such as CD83 or the production of the proinflammatory cytokines IL-12p40, IL-6, and TNF- was not detectable. Most importantly, the T cell stimulatory capacity of viral ssRNA-treated DCs was not enhanced and remained at the level of immature DCs. Taken together, our results demonstrate that viral ssRNA efficiently activates the innate defense arm of DCs, whereas it is insufficient to activate the stimulatory capacity of DCs for the adaptive defense responses.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants FWF, F2307-B13, and APP20266 from the Austrian Science Fund.

² Address correspondence and reprint requests to Dr. Johannes Stöckl, Institute of Immunology, Medical University of Vienna, Borschkegasse 8a, 1090 Vienna, Austria. E-mail address: johannes.stoeckl{at}meduniwien.ac.at

³ Abbreviations used in this paper: DC, dendritic cell; ctrl-RNA, control RNA; HRV, human rhinovirus; VPRR, viral pattern recognition receptor; RIG-I, retinoic acid inducible gene I; β-gal, β-galactosidase; poly(I:C), polyriboinosinic:polyribocytidylic acid.