The project group focuses on the immuno-suppressive properties of soluble CD83 (sCD83). Using a recombinantly expressed sCD83 molecule, it was possible to inhibit the paralyses associated with EAE, an animal model for the early, inflammatory phase of Multiple Sclerosis in a prophylactic as well as in a therapeutic setting. Furthermore, also the rejection of heart-, skin-, and cornea-transplants could be prevented by the use of sCD83. Regarding the mode of action of sCD83, we could show that it induces regulatory T cell (Treg) and that indoleamine 2,3-dioxygenase (IDO) plays a major role.
Interestingly, a naturally occurring sCD83 molecule has been identified in the serum of tumor patients, whereby high concentrations of sCD83 correlated with a reduced treatment free survival in CLL patients, indicating its relevance also in tumor patients. The therapeutic potential as well as the mode of action of sCD83 is currently under investigation using murine arthritis models as well as conditional KO animals whereby CD83 is specifically deleted only in DC, Treg, B cells as well as microglia cells. This allows the elucidation of the biological function of CD83 expression in these specific cell populations.
In addition my group is currently investigating the precise function of sCD83-mediated immune-regulatory and tolerogenic mechanisms using a murine model of cornel allograft transplantation. By detailed functional examinations we aim to elucidate, how sCD83 induced corneal allograft tolerance is maintained directly by immune cells of the donor graft and to use this knowledge to develop future therapeutic strategies.