Activation and death of immune cells during type 1 diabetes and islet transplantation
Our lab targets local immune responses for islet transplantation in type 1 diabetes and targets dendritic cells to improve or dampen immune responses. As such, molecular, cellular and whole-body immunology skills are used.
Major findings of our lab include:
the key autoantigen in autoimmune diabetes was proinsulin/insulin
peptide mimicry was identified between autoantigens in human type 1 diabetes
NOD and B6 IgG2c is an isotype, not an allotype of the BALB/c IgG2a
devising of an in vivo model of quantifying cross-presentation using selective suicide of cross-presenting dendritic cells by cytochrome c.
whereas CD40L on CD4 T cells is important for licensing dendritic cells, we showed that conversely the ability to induce CD40L on dendritic cells explains why only some viruses can elicit killer T cells in the absence of CD4 T cell help.
success in the prolongation of islet graft survival by genetic modification of islets. Recent verification that this immunosuppression is localised to the graft thereby circumventing systemic effects (susceptibility to infections) and bypassing the toxicity of transplant drugs.
We are developing new strategies to modulate immune responses for improved health outcomes.
A particular focus is on improving islet transplantation as a cure for type 1 diabetes. Currently this requires the use of dangerous immunosuppressive drugs for the transplant to be accepted. We are investigating strategies to reduce the need for systemic immunosuppression.
We are also studying how control the survival of dendritic cells and T cells. Our goal is to use this to tailor therapies to improve the outcomes for transplantation, vaccination, and treatment of autoimmune diseases.