Poster Presentation Australasian Society for Immunology Annual Scientific Meeting 2014

CD8α+ DC-B cell interaction mediated by targeted delivery of antigen to Clec9A (#353)

Yu Kato 1 , Mireille Lahoud 2 , Ken Shortman 2 3 4 , William Heath 1 , Irina Caminschi 2 3 4
  1. Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, Victoria, Australia
  2. Burnet Institute, Melbourne, VIC, Australia
  3. The Walter and Eliza Hall Institute, Parkville, VIC, Australia
  4. Department of Medical Biology, The University of Melbourne, Parkville, VIC, Australia

CD8α+ dendritic cells (DCs) are best known for their ability to crosspresent antigens to CD8+ T cells but their capacity to induce B cell responses is not widely appreciated. We have previously shown that targeted delivery of antigen to CD8α+ DCs via Clec9A induces strong humoral responses without adjuvant. Here we show that this vaccination strategy fosters direct interactions between CD8α+ DC and antigen-specific B cells.

The contribution of DC-B cell interactions to humoral responses was assessed by examining the antibody response to the B cell hapten NP conjugated to mAb against Clec9A, which, being rat IgG2a, carry effective helper T cell epitopes in mice. The potency of the anti-NP response induced by Clec9A targeting was lost when NP was instead conjugated to non-targeted isotype control mAb, even if helper T cell epitopes were delivered to Clec9A. Thus direct interactions between CD8α+ DC and NP-specific B cells contributed to induction of the anti-NP response. We then used OVA as a model protein antigen to reveal that protein antigens can be efficiently displayed and retained on the surface of CD8α+ DCs. This allowed efficient activation of antigen-specific B cells in a T cell independent manner, resulting in their accumulation along the T-B boarder within 12h of immunization. In contrast, antigen targeted to DEC205, a receptor also expressed on CD8α+ DCs, did not strongly activate antigen-specific B cells and only weakly induced antibody responses. A broader expression pattern of DEC205 by cells other than CD8α+ DCs compared to Clec9A appears to be at least partly responsible for inability to induce B cell activation.

In summary, we identified an important CD8a+ DC-B cell interaction mediated by Clec9A-targeted antigen that facilitates effective B cell activation and may be exploited in the development of next generation vaccines.