Hans U Lutz

Biology, ETH Zurich, Switzerland

Hans U Lutz

Academic positions:
- Professor and Head of the Clinical Laboratory

All industry positions (in last five years):

Research interests:
Dr Lutz's research focuses on the humoral innate immune system, comprising naturally occurring antibodies (NAbs) and the complement system. His group pioneered in studying the functional roles of NAbs in tissue homeostasis, in particular on how specific NAbs tag oxidatively stressed and senescent human red blood cells and thereby induce their phagocytosis in healthy humans and those with certain forms of anemia. More recently they have established that intravenously applied pooled human immunoglobulins (IVIG) have an anti-inflammatory effect by attenuating complement amplification in vitro and in vivo. In the course of this work they have characterized the most potent fluid phase C3/C5 convertase precursor (C3b2-IgG complexes), responsible for complement amplification. By using this precursor they built a sensitive C3 convertase assay to quantify nephritic factors and in a modified form to measue the ability of NAbs to modulate C3/C5 convertase generation. They are in the process of isolating a pair of NAbs which modulates C3/C5 convertase generation and may have a therapeutic potential in inflammatory autoimmune diseases. Another project aims at understanding how complement is amplified at the onset of a systemic inflammatory reaction (SIRS). Surprisingly this process, which can trigger a cascade of reactions leading to multi-organ failure, also involves a NAb, but with entirely different properties.

Any other information:

Any competing interests declared are displayed with individual evaluations.

Faculty Member: Hematology > Anemias & Hypocellular Marrow Disorders (since 16 January 2007)

Links

http://www.bc.biol.ethz.ch/people/groups/lutzh/

All recent recommendations

• 3.0
  Microvesicles in haemoglobinopathies offer insights into mechanisms of hypercoagulability, haemolysis and the effects of therapy.
  Recommended by Hans U Lutz
  
• 9.0
  A role of phosphatidylserine externalization in clearance of erythrocytes exposed to stress but not in eliminating aging populations of erythrocyte in mice.
  Recommended by Hans U Lutz
  
• 6.0
  Properdin binds to late apoptotic and necrotic cells independently of c3b and regulates alternative pathway complement activation.
  Recommended by Hans U Lutz
  
• 6.0
  GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak.
  Recommended by Hans U Lutz
  
• 9.0
  Hydroxyurea attenuates activated neutrophil-mediated sickle erythrocyte membrane phosphatidylserine exposure and adhesion to pulmonary vascular endothelium.
  Recommended by Hans U Lutz
  
• 9.0
  Variability and Action Mechanism of a Family of Anticomplement Proteins in Ixodes ricinus.
  Recommended by Hans U Lutz
  
• 9.0
  Microvascular endothelial cells express a phosphatidylserine receptor: a functionally active receptor for phosphatidylserine-positive erythrocytes.
  Recommended by Hans U Lutz
  
• 4.8
  Increased adhesion to endothelial cells of erythrocytes from patients with polycythemia vera is mediated by laminin alpha5 chain and Lu/BCAM.
  Recommended by Hans U Lutz, Marilyn Telen
  
• 6.0
  Activated neutrophil-mediated sickle red blood cell adhesion to lung vascular endothelium: role of phosphatidylserine-exposed sickle red blood cells.
  Recommended by Hans U Lutz