TLR-mediated stimulation of APC: Distinct cytokine responses of B cells and dendritic cells

Eur J Immunol. 2007 Nov;37(11):3040-53. doi: 10.1002/eji.200636483.


In addition to their role in humoral immunity, B lymphocytes are important antigen-presenting cells (APC). In the same way as other APC, B cells make cytokines upon activation and have the potential to modulate T cell responses. In this study, we investigated which mouse B cell subsets are the most potent cytokine producers, and examined the role of Toll-like receptors (TLR) in the control of secretion of IL-6, IL-10, IL-12 and IFN-gamma by B cells. Production of some cytokines was restricted to particular subsets. Marginal zone and B1 cells were the predominant source of B cell IL-10 in the spleen. Conversely, follicular B cells were found to express IFN-gamma mRNA directly ex vivo. The nature of the activating stimulus dramatically influenced the cytokine made by B cells. Thus, in response to combined TLR stimulation, or via phorbol esters, IFN-gamma was secreted. IL-10 was elicited by T-dependent activation or stimulation through TLR2, 4 or 9. This pattern of cytokine expression contrasts with that elicited from dendritic cells. QRT-PCR array data indicate that this may be due to differential expression of TLR signalling molecules, effectors and adaptors. Our data highlight the potentially unique nature of immune modulation when B cells act as APC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Lymphocyte Subsets
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Cytokines / metabolism*
  • DNA Primers
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Gene Expression
  • Lymphocyte Activation / immunology*
  • Mice
  • RNA, Messenger / analysis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Toll-Like Receptors / immunology*
  • Toll-Like Receptors / metabolism


  • Cytokines
  • DNA Primers
  • RNA, Messenger
  • Toll-Like Receptors