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Plasmacytoid Dendritic Cells Are Activated by Toxoplasma gondii to Present Antigen and Produce Cytokines¹

Marion Pepper^*, Florence Dzierszinski, Emma Wilson^*, Elia Tait^*, Qun Fang^*, Felix Yarovinsky, Terri M. Laufer, David Roos and Christopher A. Hunter^2,*

^* Department of Pathobiology, Department of Biology, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, Bethesda, MD 20892

Infection with the parasite Toxoplasma gondii leads to the induction of a Th1-type response dominated by IFN- production and control of this pathogen. Cells of the innate immune system are essential in initiating this response both through the production of IL-12 as well as the presentation of parasite-derived Ags to MHC-restricted T cells. Although dendritic cells (DCs) have been implicated in these events, the contribution of individual DC populations remains unclear. Therefore, multiparameter flow cytometry was used to identify and characterize subsets of murine DCs during acute toxoplasmosis. This approach confirmed that infection leads to the expansion and activation of conventional DC (cDC) subsets. Unexpectedly, however, this analysis further revealed that plasmacytoid DCs are also expanded and that these cells up-regulate MHC class II and costimulatory molecules associated with their acquired ability to prime naive CD4⁺ T cells. Furthermore, T. gondii-activated plasmacytoid DCs produce high levels of IL-12 and both plasmacytoid DC maturation and cytokine production are dependent on TLR11. Together these studies suggest that pDCs are a prominent DC subset involved in the initial stages of T. gondii infection, presenting parasite Ags and producing cytokines that are important for controlling infection.

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 National Institutes of Health Grants AI 071302 and 42334, the State of Pennsylvania, and the Mari Lowe Center (to C.A.H.).

² Address correspondence and reprint requests to Dr. Christopher A. Hunter, Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Room 313, Hill Pavillion, 380 South University Avenue, Philadelphia, PA 19104. E-mail address: chunter{at}phl.vet.upenn.edu

³ Abbreviations used in this paper: DC, dendritic cell; pDC, plasmacytoid DC; STAg, soluble Toxoplasma Ag; cDC, conventional DC; RFP, red fluorescent protein; mfi, mean fluorescent intensity.