Our mission

We aim at understanding the multiple phenotypes of innate immune cells, among them, macrophages. It is our intention to elucidate biochemical signatures of macrophages during onset and resolution of inflammation and to apprehend their multiple roles in the tumor microenvironment.

Acute and chronic inflammation as well as smoldering inflammation in the tumor microenvironment is relevant for a number of life threatening diseases, demanding basic and translational-orientated biomedical research in the area of Pathobiochemistry. We work towards a better understanding of the pathogenesis and therapeutic interventions of inflammatory conditions and tumor progression.



Onset and resolution of inflammation as well as the pro- versus anti-tumor microenvironment is controlled, at least to a major extent, by resident and infiltrating immune cells, e.g. macrophages. Their extreme plasticity is shaped by the ability to sense multiple micro-environmental incoming signals and to deliver a dynamic continuum of output responses.

We assume that the controlled transition from a classically activated or pro-resolving to an alternatively activated macrophage phenotype is fundamental to understand how inflammation resolves and why tumors progress towards malignancy. Basic to this decision making process is the removal of dying cells, i.e. apoptotic cells by macrophages. Defects in removing cellular debris by myeloid phagocytes prominently adds to the induction and propagation of inflammation, while in the tumor context apoptotic tumor cells condition macrophages to support tumor growth and survival.

To comprehend the full dynamic range of macrophage responses during inflammation and in the tumor context we aim at understanding

  • How various incoming signals shape the macrophage phenotype and
  • How polarized macrophages communicate with their microenvironment
Macrophage Phenotype



Specifically, our work seeks to define:

  • How chronic hypoxia affects the genomic, proteomic, and metabolomic landscape of macrophages
  • How apoptotic cells and signals derived from dying cells shape the macrophage phenotype. This includes lipid mediators (sphingosine-1-phosphate), miRNAs, and cytokines (IL-38)
  • How lipid metabolizing enzymes (ALOX5, ALOX15, mPGES1, PTDSS1, ACLY) regulate macrophage biology
  • How the tumor microenvironment controls translation and the ability of macrophages to store or release iron


Synopsis of Research Themes


Funding (over the last years is provided by):

  • Deutsche Forschungsgemeinschaft
    (Collaborative Research Centers, Graduate Schools, individual funding)
  • Deutsche Krebshilfe
  • Wilhelm-Sander-Stiftung
  • LOEWE (Landes Offensive zur Entwicklung Wissenschaftlich-ökonomischer Exzellenz)
  • Industry


Privacy policy    Imprint