Innate Immunity Group

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Elke Pogge von Strandmann studierte von 1986-1991  Biologie an der Friedrich-Wilhelms-Universität in Bonn und an der Ruhr Universität Bochum.

In ihrer Doktorarbeit an der Uniklinik Essen, Institut für Zellbiologie und Tumorforschung (Abteilung Prof. G.U. Ryffel, Direktor Prof. M. Rajewsky) arbeitete sie an entwicklungsbiologischen/zellbiologischen Fragestellungen. Sie promovierte 1995 mit einer Arbeit zur Differenzierung verschiedener Zelltypen in der Embryonalentwicklung. Die Habilitation an der medizinischen Fakultät wurde durch ein Lise Meitner Stipendium des Landes NRW und Drittmitteln der Deutschen Forschungsgemeinschaft gefördert. 2002 erhielt sie die Venia Legendi für das Fach Zellbiologie.

Seit 2003 setzt Elke Pogge von Strandmann ihre Forschungsarbeiten an der Klinik I für Innere Medizin der Uniklinik Köln fort. Ziel ihrer Gruppe ist die Entwicklung innovativer immuntherapeutischer Strategien zur Bekämpfung von Tumoren. Wesentlich dafür ist es, die Interaktion von Immunzellen mit Tumorzellen auf molekularer Ebene zu verstehen. Im Rahmen dieses Forschungsschwerpunktes liegt der Fokus insbesondere auf der angeborenen Immunabwehr und den Rezeptoren und Liganden, die die Erkennung von Tumorzellen steuern.


  • Biologie von NK Zellen
  • Rezeptor-Ligand Interaktionen
  • Immunliganden: therapeutische Antikörperkonstrukte
  • Tumor Microenvironment

Research Interests

NK cells are a major component of the innate immune system and critically involved in immune surveillance of tumour cells. The main interest of our group is to clarify the principles of tumour cell detection by NK cells at the molecular level, based on the example of haematological malignancies. Knowledge of the relevant receptor ligand interactions and their regulation are absolutely essential to develop NK cell-based therapeutic concepts for the treatment of tumour patients.

NK cells identify and eliminate tumour cells without prior antigen-mediated stimulation. They not only distinguish between "self" and "foreign", but also specifically seek for pathological changes such as malignant transformation of cells.

The NKG2D receptor and the group of natural cytotoxicity receptors (NCRs: NKp46, NKp44, NKp30) are regarded as important NK cell receptors in tumour defence. The outstanding significance of these receptors is very impressively demonstrated by the fact that specific masking of the receptors with antibodies inhibits the lysis of tumour cells. In haematological neoplasias, the expression of the corresponding ligands is correlated with the recognition and killing by autologous NK cells. Loss of ligand expression and impaired recognition by NK cells has been described in the course of tumour progression.

Immune surveillance via NKG2D/NKG2D-L interactions appears to be particularly effective in the early stages of tumour growth. Thus, the inducible surface expression of NKG2D ligands after DNA damage is regarded as an early "stress signal" from cells and indicative for mutations even before malignant transformation occurs. Persistent surface expression of ligands on target cells and the proteolytic formation of soluble ligands, on the other hand, may inhibit the specific immune response and enhance tumour progression.

The class of NCRs belongs to the superfamily of immunoglobulin-like molecules (NKp30, NKp44, NKp46 and the Co-receptor NKp80) Expression of these receptors has been detected only on NK cells. NKp30 and NKp46 occur on resting and activated cells whereas NKp44 is only expressed after stimulation e.g. with interleukin 2. The trans-membrane domains and intercellular regions of these receptors contain no typical sequence motives, such as ITAMs, which interact with known signal chains. However, they possibly associate with CD3 or FcR adapter molecules, which are phosphorylated in vitro after antibody-mediated networking of the receptors with tyrosine residues. The cellular ligands of NCRs are still largely unknown or poorly characterised.

There is increasing evidence that transformed cells secrete ligands for the NCRs expressed on NK cells to alert the innate immune system to the dangerous cell. The significance of these largely unknown, secreted factors for target cell identification and stimulation of NK cell activity was only recently described in a small number of articles. These data show that there is a type of target cell recognition beyond "missing self" and "induced self" that depends on extracellular factors, that are released from damaged or stressed cells ("danger induced").

We use leukemia mouse models and primary cells from humans and mice to specifically elucidate the role of cellular stress such as genetic lesions and the cellular DNA damage response for the immune alert via surface expression and/or release of ligands engaging NK cell receptors.

Immune cells are often recruited into the malignant tissue, where they are reprogammed not to damage the malignant cells but to support tumour growth. It is largely unknown how malignant cells communicate with host immune cells in trans. The focus of Priv.-Doz. Dr. Hinrich Hansen is to explore the mechanism how malignant cells interact with distant (not directly neighboring) mast cells, granulocytes or monocytes in tumour tissue. We study the following mechanisms: metalloproteinase-dependent receptor or ligand shedding, extracellular microvesicle release and tubular networks. The primary aim is to understand this tumour-supporting interaction and to explore innovative therapeutic options.        

The following specific questions are currently addressed:

  • Aim 1: Identification of novel ligands for activating NK cell receptors, which act as danger signals.
  • Aim 2: Analysis of extracellular microvesicles that present or transfer ligands for NK cell receptors in healthy individuals, tumour patients and animal models.
  • Aim 3: Elucidation of the pathways responsible for the biogenesis of immune suppressive or immune stimulatory microvesicles.
  • Aim 4: Transfer of the results to clinical applications: Role of tumour released microvesicles for the establishment and maintenance of the tumour microenvironment.
  • Aim 5: Transfer of the results to clinical applications: Development of recombinant, bispecific and trispecific proteins (immunoligands) that target NK cells via an activating receptor and tumour cells via an antibody-derived singe chain (e.g. CD19, CD33) for the immunotherapy of tumours.

Lab members

Lab Martina Bessler, TA
Teresa Bösl, PhD Student
Maria Dams, PhD Student
Hinrich Hansen, Priv.-Doz. Dr. rer. nat.
Alina Herrmann, Master Student
Manuela Klaas, Master Student
Anne Krüssmann, TA
Silke Modersohn, TA
Katrin Reiners, Dr. rer. medic.
Maike Sauer, PhD Student
Olga Shatnyeva, Dr. rer. nat.
Gisela Schön, TA
Maulik Vyas, PhD Student

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