Activation of DC via dectin-1/syk pathways in relation to CD4 T cell priming

We have obtained data from in vitro studies to demonstrate that DC can be activated via the dectin-1/Syk pathway to become APC capable of priming CD8+ T cells. In addition, we have shown that the same DC can interact with Tregs and convert them into cells that co-express ROR?t and Foxp3 and produce IL-17.
We have shown that this pathway can serve as an alternative to TLR signalling for allowing DC to become effector cells capable of priming CD4+ T cells. We have used agonists of the dectin-1/Syk pathway as adjuvants in vivo to induce DC activation and CD4+ T cell and antibody responses. We have shown that this operates in a dectin-1-dependent manner. We have also found induction of T-independent antibody responses via the same pathway. In addition, we have shown that tubulovesicular structures generated by cells overexpressing VSV-G act as adjuvants for inducing CD8+ and CD4+ T cell, as well as antibody responses in vivo. This is likely due to their DNA content and ability to trigger TLR9.

We will continue to use DC activation in vitro and, in particular, DC cytokine production as an assay to dissect innate pathways involved in DC activation. In parallel, we will continue to compare effector T cell instruction by DC activated via distinct innate receptors.

• molecule type
• regulatory t cell,
• CD8,
• FOXP3 gene,
• dectin-1,
• Toll like receptor,
• CD4

• cell type
• T cell,
• dendritic cell

• experimental design type
• in vitro design experiment

created over 16 years ago (2 March 2009)    last modified over 13 years ago (28 September 2011)   [ RDF ]   [ RelFinder ]