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 Blood, 1 March 2006, Vol. 107, No. 5, pp. 2022-2029.
Prepublished online as a Blood First Edition Paper on November 3, 2005; DOI 10.1182/blood-2005-05-2016.

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IMMUNOBIOLOGY

CD11c+ dendritic cells and plasmacytoid DCs are activated by human cytomegalovirus and retain efficient T cell-stimulatory capability upon infection

Espen Ø. Kvale, Jakob Dalgaard, Fridtjof Lund-Johansen, Halvor Rollag, Lorant Farkas, Karsten Midtvedt, Frode L. Jahnsen, Jan E. Brinchmann, and Johanna Olweus

From the Institute of Immunology and the Institute of Medical Microbiology, Oslo; and the Laboratory for Immunohistochemistry and Immunopathology at the Institute of Pathology, the Section of Nephrology at the Department of Medicine, and the Section of Hematology at the Department of Medicine, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway.

It has been suggested that human cytomegalovirus (HCMV) evades the immune system by infecting and paralyzing antigen-presenting cells. This view is based mainly on studies of dendritic cells (DCs) obtained after culture of monocytes (moDCs). It is contradicted by the asymptomatic course of HCMV infection in healthy persons, indicating that other key antigen-presenting cells induce an efficient immune response. Here we show that HCMV activates CD11c+ DCs and plasmacytoid DCs (PDCs). In contrast to moDCs, CD11c+ DCs and PDCs produced interferon (IFN) type 1 when exposed to HCMV. Autocrine IFN type 1 partially protected CD11c+ DCs against infection, whereas PDCs were resistant to HCMV even when IFN type 1 activity was inhibited. HCMV exposure induced the maturation of CD11c+ DCs by IFN type 1-dependent and -independent mechanisms. Importantly, CD11c+ DCs infected by inhibiting IFN type 1 activity retained full capacity to stimulate T cells. Renal transplant recipients receiving immunosuppressive treatment had lower frequencies of CD11c+ DCs and PDCs in blood than did healthy controls. The results show that HCMV activates the immune system by interacting with CD11c+ DCs and PDCs and that recipients of renal transplants have low frequencies of these cell types in blood.


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