Systems-oriented immunology and inflammation research
The idea that death can save lives is indeed a truism, but for complex organisms there is a significant protective mechanism in the background. Apoptosis is the name for the “suicide programme”, with which injured, old, mutated or dangerous cells can be deactivated in human tissue. But this suicide program can be misused by pathogens – or it can get out of control. You can read here how scientists are seeking to understand and make use of programmed cellular death in a cooperative research group within the Institute for Molecular and Clinical Immunology at the Otto-von-Guericke University Magdeburg and the HZI.
In the course of evolution, organisms that consist of more than one cell have developed various mechanisms for killing their own cells in a targeted manner. These mechanisms are triggered according to occasion and cell type and are acutely sensitive to environmental influences. Such a “suicide programme” for cells is called apoptosis. It is responsible for the elimination of injured, old, mutated or dangerous cells, as well as for self-regulation of tissues.
And it plays an important role in the interaction between pathogens and the host cell. For example, immune cells in infected tissue cells release apoptosis in order to inhibit further reproduction of the pathogens – because viruses in dead cells cannot reproduce. On the other hand, certain viruses and bacteria can also inhibit apoptosis in the host cell, in order to assure their own survival.
Also, when regulation of apoptosis within the organism has been interrupted, illnesses can arise. If apoptosis has, for example, been limited, this can lead to a breakdown of tolerance mechanisms and ultimately to an auto-immune disease; this disease causes the immune system to turn on the organism itself. In order to better understand these mechanisms, our scientists are decoding these signaling pathways, which regulate apoptosis in the cells of the immune system.
Bachelor & Master
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- Gas und Bremse für Immunantworten
Unser Immunsystem ist geprägt durch ein kompliziertes Wechselspiel unterschiedlicher Immunzellen, das Wissenschaftler stückchenweise verstehen lernen. Um das Immunsystem daran zu hindern, dass es sich gegen uns selbst richtet oder um ihm auch mal einen Schubs geben zu können, müssen sie die molekularen Stellknöpfe finden – und beeinflussen. Einen dieser Stellknöpfe haben Ingo Schmitz und Marc Schuster entdeckt. Folgen Sie den beiden ins Labor...