Treatment of AML by allogeneic stem cell transplantation is mediated by T cells but is hampered by a high mortality rate. We find that T-cell function is modulated through progressively evolving changes in phenotype and function of AML. Our goal is to unravel changes in T-cell responses and develop multi-specific anti¬body derivatives (msADs), tailored to interfere with immune checkpoint molecules in specific geno- and phenotype of AML subtypes.
DFG Programme
Research Grants
