IFN-α produced by human plasmacytoid dendritic cells enhances T cell-dependent naïve B cell differentiation

J Leukoc Biol. 2011 Jun;89(6):811-21. doi: 10.1189/jlb.0810460. Epub 2011 Jan 13.


The development and quality of a humoral immune response are largely influenced by the environment that supports the activation of naïve B cells. Human PDCs, through their unique capacity to produce high levels of IFN-α, have been shown earlier to enhance B cell responses stimulated by selected TLR ligands. In this study, we investigated whether PDCs also promote B cell activation induced by Th cell interactions and BCR ligation. Sorted human naive CD19(+) CD27(-) B cells were activated in vitro with anti-Ig and irradiated CD4(+) T cells. Under these conditions, the presence of supernatants from TLR-stimulated PDCs increased B cell proliferation, the frequency of B cells that differentiated to CD27(high) CD38(high) cells, and secretion of IgM. Similar results were observed when the B cells were activated in the presence of purified IFN-α. In contrast, supernatants from stimulated MDCs did not augment these functions. Also, IFN-α treatment of B cells up-regulated the expression of costimulatory molecule CD86 but not CD40, CD80, MHC class II, or CD25. Although direct IFN-α exposure of T cells suppressed their proliferative capacity, IFN-α treatment of B cells led to a small increase in their capacity to induce superantigen-driven activation of autologous CD4(+) T cells. In summary, PDCs, via their production of IFN-α, may render B cells more responsive to T cell contact, which in turn, facilitates B cell proliferation and differentiation to antibody-producing cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibody-Producing Cells / immunology*
  • B-Lymphocytes / immunology*
  • Cell Differentiation / immunology*
  • Cells, Cultured
  • Cytokines / metabolism
  • Dendritic Cells / metabolism*
  • Humans
  • Immunoglobulin M / metabolism
  • Immunologic Memory
  • Interferon-alpha / metabolism*
  • Lymphocyte Activation
  • T-Lymphocytes / immunology*


  • Cytokines
  • Immunoglobulin M
  • Interferon-alpha