Viral infection switches non-plasmacytoid dendritic cells into high interferon producers

Sandra S. Diebold, Maria Montoya, Hermann Unger, Lena Alexopoulou, Polly Roy, Linsey E. Haswell, Aymen Al-Shamkhani, Richard Flavell, Persephone Borrow and Caetano Reis e Sousa ()
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Sandra S. Diebold: Cancer Research UK, London Research Institute
Maria Montoya: Edward Jenner Institute for Vaccine Research
Hermann Unger: University of Veterinary Medicine
Lena Alexopoulou: Yale University School of Medicine and Howard Hughes Medical Institute
Polly Roy: London School of Hygiene & Tropical Medicine
Linsey E. Haswell: The School of Medicine, Southampton General Hospital
Aymen Al-Shamkhani: The School of Medicine, Southampton General Hospital
Richard Flavell: Yale University School of Medicine and Howard Hughes Medical Institute
Persephone Borrow: Edward Jenner Institute for Vaccine Research
Caetano Reis e Sousa: Cancer Research UK, London Research Institute

Nature, 2003, vol. 424, issue 6946, 324-328

Abstract: Abstract Type I interferons (IFN-I) are important cytokines linking innate and adaptive immunity1. Plasmacytoid dendritic cells make high levels of IFN-I in response to viral infection and are thought to be the major source of the cytokines in vivo2. Here, we show that conventional non-plasmacytoid dendritic cells taken from mice infected with a dendritic-cell-tropic strain of lymphocytic choriomeningitis virus make similarly high levels of IFN-I on subsequent culture. Similarly, non-plasmacytoid dendritic cells secrete high levels of IFN-I in response to double-stranded RNA (dsRNA), a major viral signature3, when the latter is introduced into the cytoplasm to mimic direct viral infection. This response is partially dependent on the cytosolic dsRNA-binding enzyme protein kinase R4 and does not require signalling through toll-like receptor (TLR) 3, a surface receptor for dsRNA5. Furthermore, we show that sequestration of dsRNA by viral NS1 (refs 6, 7) explains the inability of conventional dendritic cells to produce IFN-I on infection with influenza. Our results suggest that multiple dendritic cell types, not just plasmacytoid cells, can act as specialized interferon-producing cells in certain viral infections, and reveal the existence of a TLR-independent pathway for dendritic cell activation that can be the target of viral interference.

Date: 2003
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DOI: 10.1038/nature01783

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