Plasmacytoid dendritic cells (pDCs) are a subset of DCs that are morphologically similar to plasma cells and can rapidly produce large amounts of type I interferons (IFNs) after exposure to viruses. Most studies on pDCs have focused on their ability to stimulate T-cell responses, but a new study from Jacques Banchereau's group shows that pDCs have a role in inducing virus-specific antibodies.
When peripheral-blood mononuclear cells (PBMCs) were depleted of pDCs before being exposed to influenza virus in vitro, this resulted in a 90% decrease in IFN-α secretion and virtually no influenza-specific antibodies were detectable by enzyme-linked immunosorbent assay. B cells co-cultured with virus, T cells or a CD40L-transfected cell line, and interleukin-2 (IL-2) produced low levels of virus-specific antibodies, but addition of 5000 pDCs resulted in a marked increase in antibody production.
To investigate the mechanism, they cultured CD40-activated B cells in transwells and showed that plasma-cell differentiation was mediated by soluble factors. These factors were identified as IFN-α/β and IL-6 because neutralization of these factors totally inhibited antibody secretion. Addition of IL-2, IL-6 and IFN-α induced the highest secretion of antibodies.
The authors suggest that when pDCs are exposed to virus, they secrete type I IFNs and become mature, antigen-presenting DCs. T cells respond by secreting IL-2 and expressing CD40L, which stimulates the pDCs to secrete IL-6 and activates B cells. Type I IFNs from the pDCs induce B cells to become plasmablasts, whereas IL-6 promotes the transition of plasmablasts into antibody-secreting plasma cells.
This study shows that in addition to their role in triggering T-cell responses, pDCs are important for generating antibody-secreting plasma cells during virus infection.
ORIGINAL RESEARCH PAPER
Jego, G. et al. Plasmacytoid dendritic cells induce plasma cell differentiation through type I interferon and interleukin 6. Immunity 19, 225–234 (2003)
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Bell, E. A new role for pDCs. Nat Rev Immunol 3, 778 (2003). https://doi.org/10.1038/nri1211
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DOI: https://doi.org/10.1038/nri1211